Alzheimer's disease is the primary cause of dementia and imposes a significant socioeconomic burden globally. Physical exercise, as an effective strategy for improving general health, has been largely reported for its effectiveness in slowing neurodegeneration and increasing brain functional plasticity, particularly in aging brains. However, the underlying mechanisms of exercise in cognitive aging remain largely unclear. Adiponectin, a cell-secreted protein hormone, has recently been found to regulate synaptic plasticity and mediate the antidepressant effects of physical exercise. Studies on the neuroprotective effects of adiponectin have revealed potential innovative treatments for Alzheimer's disease. Here, we reviewed the functions of adiponectin and its receptor in the brains of human and animal models of cognitive impairment. We summarized the role of adiponectin in Alzheimer's disease, focusing on its impact on energy metabolism, insulin resistance, and inflammation. We also discuss how exercise increases adiponectin secretion and its potential benefits for learning and memory. Finally, we highlight the latest research on chemical compounds that mimic exercise-enhanced secretion of adiponectin and its receptor in Alzheimer's disease.

Stromal vascular fraction (SVF), a heterogeneous cell population primarily derived from adipose tissue, is widely utilized in regenerative therapies for its wound-healing properties and accessibility. While its immediate availability is advantageous, repeated harvesting can be burdensome, especially for elderly patients, and the regenerative capacity of SVF declines with donor age. Long-term cryopreservation offers a potential solution by allowing the banking of SVF from younger donors for future use; however, the impact of this process on SVF functionality remains elusive. This study investigates the stemness and wound-healing potential of SVF following prolonged cryopreservation.

SVF cells were isolated from adipose tissue harvested from twelve patients and cryopreserved for either two months (short-term cryopreserved SVF, S-SVF) or 12-13 years (long-term cryopreserved SVF, L-SVF), with six patients in each group. In vitro assays assessed cell viability and stemness, while in vivo assays evaluated wound-healing ability by administering thawed SVF cells from each group to dorsal wounds in immunodeficient mice, compared with a control group. Non-parametric statistical tests analyzed the differences between groups.

L-SVF exhibited significantly lower stemness compared to S-SVF. Importantly, the L-SVF group showed significantly improved wound healing compared with the control group, although the wound-healing effect of L-SVF was inferior to that of the S-SVF.

This study demonstrated that, despite reduced stemness, L-SVF retains partial wound-healing potential after 12-13 years of cryopreservation. These findings highlight the need for optimized cryopreservation protocols to enhance SVF viability and regenerative capacity for clinical applications.

Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders affecting approximately 10% of adolescent women. According to literature data, in the case of coexistence of obesity and PCOS, menstrual cycle disorders are much more common. One of the probable reasons is the activity of adipose tissue, which secretes many types of adipokines that may have a negative impact on hormonal and metabolic functions. This article reviews the literature on the role of adipokines in the etiopathogenesis of PCOS in adolescent girls. The literature base consisted of published articles - clinical trials, meta-analyses, reviews and systematic reviews. The databases - PubMed, ScienceDirect, EMBASE were searched.

Activation of adiponectin receptors (AdipoRs) has been shown to regulate glucose and lipid metabolism in mammalian hepatocytes. However, much less is known for their roles in fish. The current study demonstrated that AdipoRon, a small-molecule activator of AdipoRs, modulated glucose and lipid metabolism in large yellow croaker. In hepatocytes of large yellow croaker, AdipoRon upregulated the mRNA expression of adipors and appl1, while increasing phosphorylation levels of AMPK and AKT. These changes indicate the activation of AdipoR-mediated signaling. Furthermore, AdipoRon promoted glucose uptake, increased intracellular glucose content, as well as upregulated genes involved in glycogen synthesis and glycolysis whereas downregulated gluconeogenesis-related genes. On the other hand, AdipoRon facilitated free fatty acid (FFA) absorption by increasing the expression of fatty acid transport genes (fat/cd36, fatp1, and fabp11). It also enhanced triglyceride (TG) synthesis, evidenced by increased triglyceride levels and upregulation of dgat2 and PPARγ, which is consistent with the effect of adiponectin (APN) in large yellow croaker. Additional evidence suggested that inhibition of PPARγ with GW9662 reduced the effects of AdipoRon on glucose uptake and lipid metabolism, indicating that PPARγ is a key mediator in these metabolic regulations. Overall, AdipoRon was found to modulate multiple metabolic processes in hepatocytes of large yellow croaker via PPARγ signaling pathway, and these findings suggested that AdipoRon might contribute to beneficial effects on metabolic homeostasis in teleosts.

Global climate change is driving rapid warming in the Pacific Arctic cold-water regions. As dominant species in these areas, the Ophiura sarsii complex suffer from ocean warming stress, resulting in altered distribution patterns, physiological behaviors, and thermotolerance. However, their molecular response mechanisms to ocean warming remain unclear. We conducted transcriptomic analyses of O. sarsii vadicola under various temperature treatments: a control group at in-situ temperature (7 °C), two warming groups at the sub-lethal temperature 19 °C for one week (short-term) and two months (long-term), and a low-temperature reference group of O. sarsii at 0 °C. The results showed that a total of 66 core differentially expressed genes (58 up-regulated, 8 downregulated) were identified, with expression patterns varying by warming duration. Ophiura sarsii vadicola exhibited a more pronounced response to long-term warming than short-term ones. Three transcription factors HMGB3, METTL19, and HEAT were identified as key regulators within the co-expression networks. Furthermore, changes in folding enzymes activity and an upregulation of protein processing and chaperone genes were observed, indicating a potential activation of the unfolded protein response in brittle stars. Elevated temperatures also induced changes in multiple energy metabolism-related pathways. These findings suggest that O. sarsii vadicola may mitigate the negative effects of ocean warming by regulating key gene expression, enhancing protein homeostasis control and energy redistribution. This study provides valuable insights into the evolution and adaptability mechanisms of cold-water species under global climate change.

Perioperative neurocognitive disorder (PND) is a significant complication affecting elderly patients after surgery, with limited effective interventions to improve its prognosis yet. We have found that decreased serum adiponectin (APN) and increased cerebrospinal fluid (CSF) lactate are involved in the pathophysiological process of PND in elderly patients. APN is known for its anti-insulin resistance property. In this study, we further explored the regulatory effects of APN on cerebral glucose metabolism in PND rats. Twelve-month-old male Sprague-Dawley rats were divided into 3 groups: the sham, PND (splenectomy) and PND+APN (50 mg/kg/day intragastrically) groups. ELISA, quantitative PCR and colorimetric analysis were conducted to analyze tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), pyruvate and lactate in serum, CSF and hippocampus. Open field and Morris water maze (MWM) tests were used to detect hippocampus-dependent cognitive function. Western blot and flow cytometry were conducted to detect neuronal apoptosis in primary hippocampal neurons. In vivo, peripheral APN administration reversed surgery-induced reductions in serum APN expression and elevated levels of cerebral lactate, the ratio of lactate/pyruvate, TNF-α and IL-1β, thereby improving cognitive performance in MWM and Open Field tests. In vitro, APN at concentrations of 2 and 10 ng/ml dose-dependently reduced lipopolysaccharide-induced caspase 3 expression and p38 phosphorylation in neurons, inhibiting apoptosis. Cerebral hypometabolism is one of the pathogenic mechanisms of PND. APN shows its effects on regulating glucose metabolism to inhibit neuroinflammation and neuronal apoptosis in PND. And the underlying mechanism of APN should be investigated further.

Multiple sclerosis (MS) is a chronic autoimmune disorder of the central nervous system (CNS), characterized by demyelination, neuroinflammation, and the progressive accumulation of neurologic deficits. Adipose tissue secretes predominantly the bioactive molecules, known as adipokines, which have drawn considerable attention for their roles in modulating immune and metabolic pathways in people with MS (PwMS). Dysregulated adipokines, such as resistin, leptin, and chemerin, induce pro-inflammatory T-cell polarization while deteriorating Blood-Brain Barrier (BBB) integrity. Adiponectin, by contrast, has both immunomodulatory and neuroprotective functions. The opposing functionality highlights the biomarker and the therapeutic potential of adipokines. Preclinical and translational findings have shed light on the role of adipokines in the pathophysiology of MS by influencing T-cell, glial, and BBB functions. In clinical settings, the assessment of adipokines can function as an indicator of prognosis and diagnosis via distinct patterns of expression. In addition, alterations to adipokine profiles through lifestyle changes and pharmaceutical treatment may complement established disease-modifying treatments (DMTs). This study has highlighted the multifaceted role of adipokines in MS management, while further studies exploring the role of adipokine-mediated immunometabolic regulation are suggested.

Emerging evidence implicates an important role for visceral fat, particularly "creeping fat," in the pathogeneses and progression of inflammatory bowel diseases (IBD), specifically Crohn's disease (CD). In this study, we aimed to explore the association between body composition, adipocytokine profiles, and disease activity in pediatric CD patients.

We recruited patients with active and quiescent CD, aged 6-18, along with age matched healthy controls. Body composition was analyzed via bio-impedance analysis, and adipocytokines were assessed by ELISA-multiplex.

Patients with active CD exhibited significantly elevated levels of adiponectin and resistin compared to healthy controls and patients in remission even upon adjustment for body composition indices. Leptin correlated only with body composition and not with disease activity. Patients with active CD had relatively higher percentage of body fat and total body fat than the other groups.

This study underscores the complex interactions between adipocytokine profiles and disease activity in CD. Further studies are needed to investigate the potential mechanistic role of adiponectin and resistin in CD pathogenesis.

This article examines the human body's adaptive responses to obesity from biological, behavioral, and evolutionary perspectives. It explores how ancient survival mechanisms, such as fat storage during scarcity, have persisted but become maladaptive in modern contexts of food abundance and sedentary lifestyles. Using the Thrifty Gene Hypothesis and General Adaptation Syndrome (GAS), the study investigates how chronic stress and genetic predispositions contribute to obesity. Chronic stress, as described in GAS, is linked to obesity through mechanisms like prolonged cortisol elevation, which promotes fat storage, particularly in the abdominal region, and disrupts hunger and satiety regulation. The article also explores the possibility that contemporary chronic stress may cause the body to buffer stressful conditions through fat accumulation. While the Thrifty Gene Hypothesis suggests that genetic traits evolved to optimize energy storage during scarcity, contributing to obesity in modern environments, it remains controversial. Critics argue that it oversimplifies obesity's causes, such as lifestyle and environmental factors. Although genetic variations influencing obesity susceptibility continue to evolve, the physiological mechanisms of fat storage and stress adaptation have remained largely unchanged since ancient times.

Omega-3 (n-3) (e.g., EPA/DHA) and omega-6 (n-6) (e.g., linoleic acid [LA]) FAs are suggested to have opposite effects on inflammation, but results are inconsistent and direct comparisons of n-3 and n-6 are lacking. In a double-blind, randomized, and crossover study, females (n = 16) and males (n = 23) aged 30-70 years with abdominal obesity were supplemented with 3-4 g/d EPA/DHA (fish oil) or 15-20 g/d LA (safflower oil) for 7 weeks, with a 9-week washout phase. Cytokines and chemokines (multiplex assay), acute-phase proteins (MALDI-TOF mass spectrometry), endothelial function (vascular reaction index), blood pressure, FA composition (red blood cell membranes/serum/adipose tissue, GC-MS/MS), and adipose gene expression (microarrays, quantitative PCR) were measured. While significant differences between treatments in relative change scores were found for systolic blood pressure (n-3 vs. n-6: -1.81% vs. 2.61%, P = 0.003), no differences between n-3 and n-6 were found for any circulatory inflammatory markers. However, compared with baseline, n-3 was followed by reductions in circulating TNF (-24.9%, P < 0.001), regulated upon activation, normal T cell expressed and secreted (-12.1%, P < 0.001), and macrophage inflammatory protein 1-beta (-12.5%, P = 0.014), and n-6 by lowered TNF (-18.8%, P < 0.001), regulated upon activation, normal T cell expressed and secreted (-7.37%, P = 0.027), monocyte chemoattractant protein-1 (-7.81%, P = 0.020), and macrophage inflammatory protein 1-beta (-14.2%, P = 0.010). Adipose tissue showed significant treatment differences in weight percent of EPA (n-3 vs. n-6: 50.2%∗ vs. -1.38%, P < 0.001, ∗: significant within-treatment change score), DHA (16.0%∗ vs. -3.67%, P < 0.001), and LA (-0.033 vs. 4.91%∗, P < 0.001). Adipose transcriptomics revealed overall downregulation of genes related to inflammatory processes after n-3 and upregulation after n-6, partly correlating with changes in circulatory markers. These data point to tissue-specific proinflammatory effects of high n-6 intake, but a net systemic anti-inflammatory effect as for n-3.

Cardiac lipotoxicity, characterized by excessive lipid accumulation in the cardiac tissue, is a critical contributor to the pathogenesis of diabetic heart. Recent research has highlighted the key mechanisms underlying lipotoxicity, including mitochondrial dysfunction, endoplasmic reticulum stress, inflammation, and cell apoptosis, which ultimately impair the cardiac function. Various therapeutic interventions have been developed to target these pathways, mitigate lipotoxicity, and improve cardiovascular outcomes in diabetic patients. Given the global escalation in the prevalence of diabetes and the urgent demand for effective therapeutic approaches, this review focuses on how targeting cardiac lipotoxicity may be a promising avenue for treating diabetes.

Background/Objectives: Growth in the aging world population is accompanied by an increase in comorbidities, profoundly impacting the quality of life of older people. This development has motivated a large effort to investigate the mechanisms underlying aging and the search for countermeasures. The most investigated strategies envisage the control of diet and physical exercise, which exploit both common and distinct mechanisms to promote health. Since the application of nutritional and exercise protocols to aged persons introduces several issues due to their disabled state, some strategies have been developed. The nutritional approach exploits a wide range of compounds, including calorie restriction mimetics, supplements, antioxidants, and others. In the context of exercise, in recent years, molecules able to provide similar effects to exercise, the so-called exercise mimetics, have been developed. Methods: To have a better perspective on exercise mimetics and their connection with nutrition, we performed a systematic search of the PubMed and Scopus databases using the term "exercise mimetics". Results: In total, 97 research articles were selected and discussed. The present review provides evidence of the presence of multiple exercise-mimetic compounds and physical strategies that can target metabolic pathways, oxidative stress defense mechanisms, or myokine modulation. Conclusions: Interestingly, this review highlights that an important number of exercise mimetics are represented by products of natural origin and supplements assimilable with diet. This evidence provides a further link between exercise and nutrition and confers a central role on nutrition in the context of exercise mimetics.

Cigarette smoke activates lung inflammation and destruction and the development of COPD. Among various factors influenced by lung inflammation, adiponectin produced by lung epithelial cells is thought to play a significant role in regulating inflammation and maintaining tissue integrity. This study aims to examine adiponectin expression in a mouse model of cigarette smoke extract (CSE)-induced emphysema and explore the effects of adiponectin on cell survival and cytokine gene expression in CSE-induced lung epithelial cell damage.

CSE was prepared by passing cigarette smoke through a glass tube containing solvent. PBS or CSE was intraperitoneally administered to C57BL/6 mice. Inflammatory cells, cytokines, adiponectin expression in lung, bronchoalveolar lavage fluid (BALF) and adipose tissue were assessed. CSE and adiponectin were administered to A549 cells to determine cell viability and cytokine gene expression.

Intraperitoneal CSE injection significantly increased the mean alveolar linear intercept by 23.11%. CSE significantly increased total cells, macrophages, neutrophils, eosinophils, TNFα, IL-1β levels in BALF. CSE enhanced lung adiponectin protein expression. Treatment of A549 cells with CSE reduced cell survival and adiponectin gene expression. Furthermore, adiponectin treatment enhanced MCP-1 and IL-8 gene expression in A549 cells post-CSE exposure.

Intraperitoneal CSE treatment induced lung inflammation, airspace enlargement, and increased adiponectin expression in mice. CSE-exposed A549 cells showed reduced cell viability, upregulated proinflammatory genes, downregulated adiponectin genes. Adiponectin treatment further intensified these genes expressions, aligning with in vivo findings. Elevated adiponectin expression in alveolar epithelial cells suggests its potential role in the development of COPD by enhancing lung inflammation.

Adiponectin is a hormone produced by adipocytes with anti-atherosclerotic and anti-diabetic properties. We previously discovered that adiponectin is specifically localized in the myoepithelial cells of rat sublingual glands. This study aims to investigate the localization of adiponectin and its receptors, AdipoR1 and AdipoR2, in adult rats, postnatally developing rats, and diabetic model rats.

We examined the localization and expression of adiponectin and its receptors by immunohistochemistry and RT-PCR in the sublingual glands of adult rats and in two diabetic rat models: Streptozotocin (STZ)-treated rats for type 1 diabetes and GK rats for type 2 diabetes.

In rat sublingual glands, adiponectin was localized in the cytoplasm of myoepithelial cells, while AdipoR1 and AdipoR2 were localized in the basolateral membrane of mucous acinar cells. In GK rats, there was a significant decrease in the immunoreactivity and mRNA levels of adiponectin, while both AdipoR1 and AdipoR2 expression levels were upregulated. In STZ-treated rats, both adiponectin and its receptors showed reduced expression.

Adiponectin acts as a paracrine factor in sublingual myoepithelial cells, influencing salivary secretion through upregulated receptors in acinar cells, particularly in type 2 diabetes. This process is associated with a reduction in myoepithelial adiponectin levels.

Although innate immunity is critical for antifungal host defense against the human opportunistic fungal pathogen Aspergillus fumigatus, potentially damaging inflammation must be controlled. Adiponectin (APN) is an adipokine produced mainly in adipose tissue that exerts anti-inflammatory effects in adipose-distal tissues such as the lung. We observed increased mortality and increased fungal burden and inflammation in neutropenic mice with invasive aspergillosis (IA) that lack APN or the APN receptors AdipoR1 or AdipoR2. Alveolar macrophages (AMs), early immune sentinels that detect and respond to lung infection, express both receptors, and APN-deficient AMs exhibited an inflammatory phenotype that was associated with decreased fungal killing. Pharmacological stimulation of AMs with AdipoR agonist AdipoRon rescued deficient killing in APN-/- AMs and was dependent on the presence of either receptor. Finally, APN-enhanced fungal killing was associated with increased activation of the non-canonical LC3 pathway of autophagy. Thus, our study identifies a novel role for APN in LC3-mediated killing of A.fumigatus.

This research was conducted to investigate the anti-obesity effects of black tea or green tea kombucha (BK, GK) and compared their compositional differences. As a result of kombucha treatment during the adipocyte differentiation process, peroxisome proliferator-activated receptor γ was significantly decreased, and CCAAT/enhancer binding protein α and adipocyte protein 2 showed a tendency to decrease with BK treatment. Oil red O staining results also demonstrated a reduction of lipid accumulation by BK treatment compared to the control. In mature adipocytes, BK significantly upregulated the gene expression of hormone-sensitive lipase and tended to increase the expression of adipose triglyceride lipase and adiponectin. Additionally, as a biomarker of lipolysis, glycerol content also marginally increased with either BK or GK treatment. The differences were observed in tea polyphenol compound and organic acid contents between BK and GK. In conclusion, these results suggest that black tea kombucha may have anti-obesity activity.

The online version contains supplementary material available at 10.1007/s10068-024-01740-8.

Understanding biological mechanisms underlying anorexia nervosa (AN) is necessary to develop care strategies. Despite many articles dedicated to peptides assessment in AN, there is no systematic review. A scoping review of circulating peptides published in relation to AN, comparing their results with those of controls, was conducted. Embase and PubMed databases were search from 1966 to 2022 (PROSPERO CRD42022323716). All original English articles, assessing peptides in AN (except classical markers) were analyzed. 1151 studies for 207 peptides, in 486 published articles were selected, and evidences/trends in AN were compared to controls. Fifteen clusters of function gathering peptides covering physiopathological aspects of AN were identified. This scoping review revealed a large variety of circulating peptides explored in AN. Some peptides presented with convincing results and helped understanding pathophysiologic aspects. Other peptides presented with nuanced results, partly due to insufficient number of studies, multiple assay techniques, inadequate sampling time, and lack of phenotyping. Conversion from bench-to-bed remains difficult and may explain why peptides evaluations did not currently lead to specific international recommendations or tailored therapeutic/preventive strategies. Peptide evaluation in anorexia nervosa could explore secretion profiles, and test it in well-phenotyped patients with AN, to conclude for potential clinical use, and finally design therapeutic tests.

Adverse childhood experiences (ACEs) are associated with a greater risk of obesity and cardiometabolic disease. Adipokines, including leptin and adiponectin, play vital roles in biological processes linked to obesity and cardiometabolic risk. The adiponectin/leptin ratio may represent a marker of impaired hormonal regulation of adipose tissue. Prior cross-sectional studies suggest patterns of higher plasma leptin and lower adiponectin among adults who have experienced ACEs. This study addresses whether ACEs influence longitudinal changes in leptin, adiponectin, and the adiponectin/leptin ratio, after accounting for current chronic stress and adiposity.

This longitudinal study included 192 middle-aged mothers (mean age = 46.78 years) experiencing higher (n = 108) and lower (n = 84) chronic caregiving stress. Adipokines and adiposity were measured at three timepoints: T1 (baseline), T2 (15 months later), and T3 (30 months after T1). ACEs were assessed retrospectively using the Childhood Trauma Questionnaire.

Mixed-effect models showed that leptin and adiponectin increased over time. Greater ACEs exposure was associated with larger increases in leptin over time, but it was not related to adiponectin or the adiponectin/leptin ratio. Current caregiving stress was not related to leptin and adiponectin levels and did not interact with ACEs in predicting adipokine levels. Mediation analyses revealed that increases in waist circumference partially mediated the association between ACEs and increases in leptin over time.

ACEs may increase vulnerability to cardiometabolic risk in midlife caregiving mothers through its influence on longitudinal changes in leptin and central adiposity.

Skeletal muscle satellite cells (SMSCs) are critical for postnatal skeletal muscle growth and regeneration. Adiponectin plays a pivotal role in regulating muscle glucose uptake and fatty acid metabolism. However, its function in the proliferation and differentiation of chicken SMSCs remains poorly understood. In this study, we investigated the effects of adiponectin on the proliferation and differentiation of in vitro cultured chicken SMSCs. Our results demonstrated that adiponectin promoted SMSCs proliferation while inhibiting myogenic differentiation and inducing adipogenic differentiation. RNA-seq analysis revealed enrichment of the MAPK signaling pathway, suggesting its potential involvement in the regulation of adiponectin on SMSCs activity. Western blot analysis revealed that adiponectin activated ERK1/2 phosphorylation and inhibited p38 phosphorylation during the process of the inhibition on myogenic differentiation in chicken SMSCs. Furthermore, suppression of ERK1/2 signaling with U0126 or activation of p38 signaling with SSK1 reversed the downregulated expression of myogenic differentiation marker MyHC, MyOD1, and MyOG induced by adiponectin. These findings validated that adiponectin impeded myogenic differentiation through activation of ERK1/2 and inhibition of p38 signaling pathways. Additionally, activation of p38 signaling pathway reduced the increased percentage of EdU-positive cells induced by adiponectin. Collectively, these findings demonstrated that adiponectin impedes myogenic differentiation of SMSCs through activating ERK1/2 and inhibiting p38 signaling pathways, while promoting proliferation by inhibiting p38 signaling pathway.

Hepatocellular carcinoma is one of the most common malignant tumors, and radiotherapy plays a pivotal role in its therapeutic regimen. However, radiotherapy resistance is the main cause of therapeutic failure in patients. Our previous study revealed that Adiponectin Receptor 1 (AdipoR1) is involved in regulating radiation resistance in liver cancer patients treated with stereotactic body radiotherapy. To explore the mechanism, we performed high-throughput transcriptome sequencing of hepatocellular carcinoma cells with stable knockdown of AdipoR1. KEGG enrichment analysis indicated that the cell cycle and ubiquitination degradation pathways may be involved in the regulation of radiation resistance by AdipoR1.The knockdown of AdipoR1 can attenuate the radiation-induced G2/M phase arrest through cyclin B1.By the ubiquitination IP assay and a rescue experiment, we confirmed that CCNB1IP1 regulated the ubiquitination and degradation of cyclin B1. Combined with information from transcription factor database and AdipoR1 transcriptome sequencing, these results showed that estrogen receptor 1 (ESR1) may be a transcription factor of CCNB1IP1. We found that AdipoR1 promoted the translocation of ESR1 from the cytoplasm to the nucleus, and ESR1 inhibited the transcription of CCNB1IP1.Therefore, we propose that AdipoR1 regulates the ubiquitination level, cell cycle progression, and radiation resistance of HCC cells through the "AdipoR1 /ESR1/CCNB1IP1/cyclin B1" axis. This study will promote the development of novel targeted radiosensitizing drugs.

The dipeptide Tyr-Pro, a novel natural agonist of adiponectin receptor 1 (AdipoR1), promotes glucose uptake in skeletal muscle cells. This study investigated the antidiabetic effect of orally administered Tyr-Pro in spontaneously diabetic Torii (SDT) rats. Oral administration of Tyr-Pro (1 mg/kg/day) improved glucose intolerance in SDT rats at 22 weeks of prediabetic age. By 29 weeks of age, fasting blood glucose levels (BGLs) increased to 142 ± 14 mg/dL in the control group, whereas those in the Tyr-Pro group remained within the normal range (80-99 mg/dL), demonstrating a novel antidiabetic effect in vivo. Substantially increased levels of AdipoR1 and p-AMPK/AMPK were observed in the skeletal muscle of Tyr-Pro-administrated SDT rats. The intake of Tyr-Pro also enhanced insulin secretion and inhibited p-IRS-1(Ser) in skeletal muscle. These findings demonstrate that Tyr-Pro prevented the onset of diabetes and improved impaired insulin signaling pathways in SDT rats by inducing AdipoR1-mediated AMPK activation.

Adiponectin is an abundantly secreted hormone that communicates information between the adipose tissue, and the immune and cardiovascular systems. In metabolically healthy individuals, adiponectin is usually found at high levels and helps improve insulin responsiveness of peripheral tissues, glucose tolerance, and fatty acid oxidation. Beyond its metabolic functions in insulin-sensitive tissues, adiponectin plays a prominent role in attenuating the development of atherosclerotic plaques, partially through regulating macrophage-mediated responses. In this context, adiponectin binds to its receptors, adiponectin receptor 1 (AdipoR1) and AdipoR2 on the cell surface of macrophages to activate a downstream signaling cascade and induce specific atheroprotective functions. Notably, macrophages modulate the stability of the plaque through their ability to switch between proinflammatory responders, and anti-inflammatory proresolving mediators. Traditionally, the extremes of the macrophage polarization spectrum span from M1 proinflammatory and M2 anti-inflammatory phenotypes. Previous evidence has demonstrated that the adiponectin-AdipoR pathway influences M1-M2 macrophage polarization; adiponectin promotes a shift toward an M2-like state, whereas AdipoR1- and AdipoR2-specific contributions are more nuanced. To explore these concepts in depth, we discuss in this review the effect of adiponectin and AdipoR1/R2 on 1) metabolic and immune responses, and 2) M1-M2 macrophage polarization, including their ability to attenuate atherosclerotic plaque inflammation, and their potential as therapeutic targets for clinical applications.

Sarcopenia is defined as a muscle-wasting syndrome that occurs with accelerated aging, while cachexia is a severe wasting syndrome associated with conditions such as cancer and immunodeficiency disorders, which cannot be fully addressed through conventional nutritional supplementation. Sarcopenia can be considered a component of cachexia, with the bidirectional interplay between adipose tissue and skeletal muscle potentially serving as a molecular mechanism for both conditions. However, the underlying mechanisms differ. Recognizing the interplay and distinctions between these disorders is essential for advancing both basic and translational research in this area, enhancing diagnostic accuracy and ultimately achieving effective therapeutic solutions for affected patients. This review discusses the muscle microenvironment's changes contributing to these conditions, recent therapeutic approaches like lifestyle modifications, small molecules, and nutritional interventions, and emerging strategies such as gene editing, stem cell therapy, and gut microbiome modulation. We also address the challenges and opportunities of multimodal interventions, aiming to provide insights into the pathogenesis and molecular mechanisms of sarcopenia and cachexia, ultimately aiding in innovative strategy development and improved treatments.

Adipokines including adiponectin (ADIPO), chemerin (CHEM) and visfatin (VISF) are involved in metabolism and reproductive functions. These 3 adipokines are present in ovarian cells in different preovulatory follicles in hens. We have previously shown that VISF and ADIPO are able to modulate in vitro steroid production by hen granulosa cells (GCs). It is, however, unclear whether CHEM acts on hen ovarian cells. In addition, no study has yet investigated the effect of a mixture of several adipokines such ADIPO, VISF, and CHEM on GCs from different preovulatory follicles. In this study, we investigated the effect of CHEM alone and in combination with ADIPO and VISF on cell viability, proliferation and progesterone secretion in cultured granulosa cells (GCs) from the largest follicles F1 and smaller ones (F3/F4) in the presence of gonadotropins (oLH and oFSH) or hIGF-1. First, various concentrations of chemerin were examined (0, 12, 25, 50, and 100 ng/mL) and then we determined the response to CHEM (at 25 ng/mL) in combination with ADIPO (10 µg/mL) and VISF (100 ng/mL). Chemerin exposure did not affect F1 and F3/F4 granulosa cell viability and proliferation whatever the concentation and in the presence of the mixture. However, it reduced progesterone secretion in dose dependent manner in both F1 and F3/F4 follicles. Furthermore, this CHEM inhibitory effect was significantly higher when CHEM was combined with ADIPO and VISF. Furthermore, CHEM reduced significantly oLH and oFSH- induced progesterone secretion in F1 GCs and oFSH and hIGF-1-induced progesterone secretion in F3/F4 GCs. Interestingly, this inhibitory effect of CHEM was similar in F1 GCs when CHEM was in mixture with ADIPO and VISF whereas it was significantly higher in F3/F4 GCs. Taken together, CHEM impairs progesterone secretion in cultured hen GCs and this inhibitory effect can be potentiated when it is in combination with other adipokines.

Benign prostatic hyperplasia (BPH), a common cause of lower urinary tract symptoms (LUTS), has been recently regarded as a metabolic disease. Metabolic syndrome (MetS) is a constellation of metabolic disarrangements, including insulin resistance, obesity, hypertension, and dyslipidemia, and it has been established that these components of MetS are important contributing factors exacerbating the degree of prostatic enlargement and bladder outlet obstruction among patients with BPH. Clinical and experimental studies demonstrated that many molecules, such as insulin, insulin-like growth factor 1 (IGF-1), androgen and estrogen, and adipokines, are involved in the overlapping pathogenesis of BPH and MetS, indicating that clinicians might be able to simultaneously alleviate or cure two diseases by choosing appropriate medications. This article aims to systematically review the pathophysiological aspect and traditional etiology and pathogenesis of BPH and discuss the intricate association between MetS and BPH from the molecular point of view, in an attempt to provide stronger evidence for better treatment of two diseases.

The aim of this study was to investigate the relationship between serum adiponectin and leptin levels, which are cytokines released from fatty tissue, and pain, function and intervertebral disc degeneration (IVDD).

Between January 2018 and November 2019, a total of 85 patients (34 males, 51 females; mean age: 42.1±10.7 years; range, 18 to 62 years) who were diagnosed with IVDD and 84 healthy volunteers (34 males, 50 females; mean age: 41.9±10.7 years; range, 22 to 64 years) were included in this cross-sectional study. The Visual Analog Scale (VAS, 0-10 cm) and Oswestry Disability Index (ODI) scales were used in the patient group. Serum adiponectin and leptin levels were measured in all participants. The grading of IVDD was determined using the Pfirrmann Classification.

There was no significant difference in serum adiponectin (p=0.35) and leptin (p=0.19) levels between the patient group and the control group. No relationship was found between serum adiponectin and leptin levels and pain intensity (VAS), pain duration, and disability (ODI) in patients with low back pain. No relationship was found between the severity of IVDD as evidenced by magnetic resonance imaging (MRI) and adiponectin (p=0.18) and leptin (p=0.11) levels. There was a positive correlation between the severity of disc degeneration and body mass index (r=0.35, p=0.008) and waist circumference (r=0.34, p=0.01).

Serum adipokine levels were not associated with low back pain symptoms and IVDD severity as evidenced by MRI. These findings suggest that the effects of obesity on chronic low back pain and disc degeneration cannot be explained by systemic inflammatory effects alone.

The Aedes aegypti mosquito plays a critical role in the transmission of viral diseases, including Zika virus, which poses significant public health challenges. Understanding the complex interactions between mosquitoes and viruses is paramount for the development of effective control strategies. In this study, we demonstrate that silencing the A. aegypti adiponectin receptor-like protein (AaARLP) results in a reduction of Zika virus infection. Transcriptomic analysis identified alterations in several trypsin genes and further revealed that AaARLP-knockdown mosquitoes had diminished trypsin activity. Moreover, silencing of selected trypsins resulted in a similar delay in Zika virus infection in mosquitoes, further highlighting the connection between the AaARLP and trypsin. Overall, our findings demonstrate that AaARLP signaling is important for Zika virus infection of A. aegypti.

Arboviruses pose a significant threat to public health, with mosquitoes, especially Aedes aegypti, being a major vector for their transmission. Gaining insight into the complex interaction between mosquitoes and viruses is essential to build successful control strategies. In this study, we identified a novel pathway connecting the A. aegypti adiponectin receptor-like protein and its association with trypsin, key enzymes involved in blood digestion. Furthermore, we demonstrated the significance of signaling via the adiponectin receptor-like protein in virus infection within the mosquito. Together, our discoveries illuminate mosquito metabolic pathways essential in viral infection.

Obesity is one of the most prevalent and increasing metabolic disorders and is considered one of the twelve risk factors for dementia. Numerous studies have demonstrated that obesity induces pathophysiological changes leading to cognitive decline; however, the underlying molecular mechanisms are yet to be fully elucidated. Various biochemical processes, including chronic inflammation, oxidative stress, insulin resistance, dysregulation of lipid metabolism, disruption of the blood-brain barrier, and the release of adipokines have been reported to contribute to the accumulation of senescent neurons during obesity. These senescent cells dysregulate neuronal health and function by exhibiting a senescence-associated secretory phenotype, inducing neuronal inflammation, deregulating cellular homeostasis, causing mitochondrial dysfunction, and promoting microglial infiltration. These factors act as major risks for the occurrence of neurodegenerative diseases and cognitive decline. This review aims to focus on how obesity upregulates neuronal senescence and explores both pharmacological and non-pharmacological interventions for preventing cognitive impairments, thus offering new insights into potential therapeutic strategies.

Despite all the progress made by science in the prevention and treatment of cardiovascular diseases and cancers, these are still the main reasons for hospitalizations and death in the Western world. Among the possible causes of this situation, disorders related to hyperinsulinemia and insulin resistance (Hyperin/IR) are still little-known topics. An analysis of the literature shows that this condition is a multiple risk factor for type 2 diabetes, cardiovascular diseases, cellular senescence and cancer, and neurodegenerative diseases. Hyperin/IR is progressively increasing worldwide, and its prevalence has now exceeded 50% of the general population and in overweight children. Asymptomatic or poorly symptomatic, it can last for many years before manifesting itself as diabetes, cardiovascular disease, neoplasm, cognitive deficit, or dementia, therefore leading to enormous social and healthcare costs. For these reasons, a screening plan for this pathology should be implemented for the purpose of identifying people with Hyperin/IR and promptly starting them on preventive treatment.

The number of major operations performed in obese patients is expected to increase given the growing prevalence of obesity. Obesity is a risk factor for a range of postoperative complications including perioperative neurocognitive disorders. However, the mechanisms underlying this vulnerability are not well defined. We hypothesize that obese subjects are more vulnerable to general anaesthesia induced neurotoxicity due to reduced levels of adiponectin. This hypothesis was tested using a murine surgical model in obese and adiponectin knockout mice exposed to the volatile anaesthetic agent sevoflurane.

Obese mice were bred by subjecting C57BL/6 mice to a high fat diet. Cognitive function, neuroinflammatory responses and neuronal degeneration were assessed in both obese and lean mice following exposure to 2 h of sevoflurane to confirm sevoflurane-induced neurotoxicity. Thereafter, to confirm the role of adiponectin deficiency in, adiponectin knockout mice were established and exposed to the sevoflurane. Finally, the neuroprotective effects of adiponectin receptor agonist (AdipoRon) were examined.

Sevoflurane triggered significant cognitive dysfunction, neuroinflammatory responses and neuronal degeneration in the obese mice while no significant impact was observed in the lean mice. Similar cognitive dysfunction and neuronal degeneration were also observed in the adiponectin knockout mice after sevoflurane exposure. Administration of AdipoRon partially prevented the deleterious effects of sevoflurane in both obese and adiponectin knockout mice.

Our findings demonstrate that obese mice are more susceptible to sevoflurane-induced neurotoxicity and cognitive impairment in which adiponectin deficiency is one of the underlying mechanisms. Treatment with adiponectin receptor agonist ameliorates this vulnerability. These findings may have therapeutic implications in reducing the incidence of anaesthesia related neurotoxicity in obese subjects.

Endometrial receptivity is essential for successful embryo implantation and pregnancy initiation and is regulated via various signaling pathways. Adiponectin, an important adipokine, may be a potential regulator of reproductive system functions. The aim of the present study was to elucidate the regulatory role of adiponectin receptor 1 (ADIPOR1) in endometrial receptivity. The endometrial receptivity between RL95‑2 and AN3CA cell lines was confirmed using an in vitro JAr spheroid attachment model. 293T cells were transfected with control or short hairpin (sh)ADIPOR1 vectors and RL95‑2 cells were transduced with lentiviral particles targeting ADIPOR1. Reverse transcription‑quantitative PCR and immunoblot assays were also performed. ADIPOR1 was consistently upregulated in the endometrium during the mid‑secretory phase compared with that in the proliferative phase and in receptive RL95‑2 cells compared with that in non‑receptive AN3CA cells. Stable cell lines with diminished ADIPOR1 expression caused by shRNA showed reduced E‑cadherin expression and attenuated in vitro endometrial receptivity. ADIPOR1 regulated AMP‑activated protein kinase (AMPK) activity in endometrial epithelial cells. Regulation of AMPK activity via dorsomorphin and 5‑aminoimidazole‑4‑carboxamide ribonucleotide affected E‑cadherin expression and in vitro endometrial receptivity. The ADIPOR1/AMPK/E‑cadherin axis is vital to endometrial receptivity. These findings can help improve fertility treatments and outcomes.

Adiponectin regulates steroid production and influences gonadal development. This study examined the effects of tannic acid (TA) on the adiponectin levels and gonads of male Brandt's voles. Male Brandt's voles aged 90 d were randomly separated into three groups: a control group (provided distilled water), a group given 600 mg∙kg-1 TA, and a group that received 1200 mg∙kg-1 TA (continuous gavage for 18 d). In this study, we examined the effects of TA on the adiponectin, antioxidant, and inflammatory levels in the testes. Furthermore, we examined the expression of important regulatory elements that influence adiponectin expression and glucose utilisation. In addition, the body weight, reproductive organ weight, and testicular shape were assessed. Our study observed that TA treatment increased serum adiponectin levels, DsbA-L and Ero1-Lα transcription levels, and AdipoR1, AMPK, GLUT1, and MCT4 expression levels in testicular tissue. TA enhanced pyruvate and lactic acid levels in the testicular tissue, boosted catalase activity, and reduced MDA concentrations. TA reduced the release of inflammatory factors in the testicular tissues of male Brandt's voles. TA increased the inner diameter of the seminiferous tubules. In conclusion, TA appears to stimulate adiponectin secretion and gonadal growth in male Brandt's voles while acting as an antioxidant and anti-inflammatory agent.

This study aims to fill the knowledge gap regarding the effects of high frequency facial neuromuscular electrical stimulation (fNMES) on facial aging, using a device equipped with CERTEC (Cell Energy Regeneration Technology) operating between 40 and 190 kHz.

This prospective split-face study was conducted at Tokyo University Hospital between March and May 2023 with 24 healthy adult women aged 30-59. The intervention group used the fNMES device along with basic skin care on one side of the face, and basic skin care alone on the other side for 8 weeks. Evaluations included changes in skin wrinkles, sagging, and blood flow.

This study found significant improvements in skin elasticity and degree of wrinkles in the areas intervened with fNMES (p < 0.05, respectively). In addition, the intervention resulted in significant improvements in jawline angle (p < 0.01), submental volume (p < 0.05), cheek volume (p < 0.05), maximum nasolabial fold depth (p = 0.03), and total volume of the nasolabial folds (p = 0.03). The fNMES intervention also showed improvement in blood flow (p < 0.05). These improvements were also subjectively assessed by the participants in subject questionnaires at 8 weeks after the intervention (p < 0.05).

This study suggests that high frequency fNMES effectively improves facial skin elasticity, reduces wrinkles and sagging, promotes blood flow, and contributes to overall facial appearance rejuvenation. Although further studies are needed, high frequency fNMES appeared promising as a noninvasive anti-aging therapy.

Background/Objectives. A Mediterranean diet (MD) has been associated with neuroprotective effects. We aimed to assess the MD's association with stroke prognosis and the potential mediators involved. Methods. Seventy patients with acute anterior circulation ischemic stroke were included. Dietary patterns were evaluated using the MEDAS scale, a food-frequency questionnaire, and a 24 h recall. Circulating biomarkers including insulin resistance (HOMA index), adipokines (resistin, adiponectin, leptin), choline pathway metabolites (TMAO, betaine, choline), and endothelial progenitor cells (EPCs) were measured. Early neurological improvement (ENI) at 24 h, final infarct volume, and functional outcome at 3 months were assessed. Results. Adherence to MD and olive oil consumption were associated with a lower prevalence of diabetes and atherothrombotic stroke, and with lower levels of fasting glycemia, hemoglobinA1C, insulin resistance, and TMAO levels. Monounsaturated fatty acids and oleic acid consumption correlated with lower resistin levels, while olive oil consumption was significantly associated with EPC mobilization. Multivariate analysis showed that higher MD adherence was independently associated with ENI and good functional prognosis at 3 months. EPC mobilization, lower HOMA levels, and lower resistin levels were associated with ENI, a smaller infarct volume, and good functional outcome. Conclusions. MD was associated with better prognosis after ischemic stroke, potentially mediated by lower insulin resistance, increased EPC mobilization, and lower resistin levels, among other factors.

The metabolic syndrome phenotype of individuals with obesity is characterized by elevated levels of triglyceride-rich lipoproteins and remnant particles, which have been shown to be significantly atherogenic. Understanding the association between adipokines, endogenous hormones produced by adipose tissue, and remnant cholesterol (RC) would give insight into the link between obesity and atherosclerotic cardiovascular disease.

We studied 1791 MESA (Multi-Ethnic Study of Atherosclerosis) participants who took part in an ancillary study on body composition with adipokine levels measured (leptin, adiponectin, and resistin) at either visit 2 or visit 3. RC was calculated as non-high-density lipoprotein cholesterol minus low-density lipoprotein cholesterol, measured at the same visit as the adipokines, as well as subsequent visits 4 through 6. Multivariable-adjusted linear mixed-effects models were used to assess the cross-sectional and longitudinal associations between adipokines and log-transformed levels of RC. Mean±SD age was 64.5±9.6 years; mean±SD body mass index was 29.9±5.0 kg/m2; and 52.0% were women. In fully adjusted cross-sectional models that included body mass index, diabetes, low-density lipoprotein cholesterol, and lipid-lowering therapy, for each 1-unit increment in adiponectin, there was 14.6% (95% CI, 12.2-16.9) lower RC. With each 1-unit increment in leptin and resistin, there was 4.8% (95% CI, 2.7-7.0) and 4.0% (95% CI, 0.2-8.1) higher RC, respectively. Lower adiponectin and higher leptin were also associated with longitudinal increases in RC levels over median follow-up of 5 (interquartile range, 4-8) years.

Lower adiponectin and higher leptin levels were independently associated with higher levels of RC at baseline and longitudinal RC increase, even after accounting for body mass index and low-density lipoprotein cholesterol.

In pigs, meat quality depends markedly on the fatty acid (FA) content and composition of the intramuscular fat, which is partly determined by the gene expression in this tissue. The aim of this work was to identify the link between muscle gene expression and its FA composition. In an (Iberian × Duroc) × Duroc backcrossed pig population, we identified modules of co-expressed genes, and correlation analyses were performed for each of them versus the phenotypes, finding four relevant modules. Two of the modules were positively correlated with saturated FAs (SFAs) and monounsaturated FAs (MUFAs), while negatively correlated with polyunsaturated FAs (PUFAs) and the omega-6/omega-3 ratio. The gene-enrichment analysis showed that these modules had over-representation of pathways related with the biosynthesis of unsaturated FAs, the Peroxisome proliferator-activated receptor signalling pathway and FA elongation. The two other relevant modules were positively correlated with PUFA and the n-6/n-3 ratio, but negatively correlated with SFA and MUFA. In this case, they had an over-representation of pathways related with fatty and amino acid degradation, and with oxidative phosphorylation. Using a graphical Gaussian model, we inferred a network of connections between the genes within each module. The first module had 52 genes with 87 connections, and the most connected genes were ADIPOQ, which is related with FA oxidation, and ELOVL6 and FABP4, both involved in FA metabolism. The second module showed 196 genes connected by 263 edges, being FN1 and MAP3K11 the most connected genes. On the other hand, the third module had 161 genes connected by 251 edges and ATG13 was the top neighbouring gene, while the fourth module had 224 genes and 655 connections, and its most connected genes were related with mitochondrial pathways. Overall, this work successfully identified relevant muscle gene networks and modules linked with FA composition, providing further insights on how the physiology of the pigs influences FA composition.

Alzheimer's disease (AD) is a degenerative brain disease that affects millions of people worldwide. It is caused by abnormalities in cholinergic neurons, oxidative stress, and inflammatory cascades. The illness is accompanied by personality changes, memory issues, and dementia. Metabolic signaling pathways help with fundamental processes like DNA replication and RNA transcription. Being adaptable is essential for both surviving and treating illness. The body's metabolic signaling depends on adipokines, including adiponectin (APN) and other adipokines secreted by adipose tissues. Energy homeostasis is balanced by adipokines, and nutrients. Overconsumption of nutrients messes with irregular signaling of adipokines, such as APN in both peripheral and brain which leads to neurodegeneration, such as AD. Despite the failure of traditional treatments like memantine and cholinesterase inhibitors, natural plant bioactive substances like Osmotin (OSM) have been given a focus as potential therapeutics due to their antioxidant properties, better blood brain barrier (BBB) permeability, excellent cell viability, and especially nanoparticle approaches. The review highlights the published preclinical literature regarding the role of OSM in AD pathology while there is a need for more research to investigate the hidden therapeutic potential of OSM which may open a new gateway and further strengthen its healing role in the pathogenesis of neurodegeneration, especially AD.

Although innate immunity is critical for antifungal host defense against the human opportunistic fungal pathogen Aspergillus fumigatus, potentially damaging inflammation must be controlled. Adiponectin (APN) is an adipokine produced mainly in adipose tissue that exerts anti-inflammatory effects in adipose-distal tissues such as the lung. We observed 100% mortality and increased fungal burden and inflammation in neutropenic mice with invasive aspergillosis (IA) that lack APN or the APN receptors AdipoR1 or AdipoR2. Alveolar macrophages (AMs), early immune sentinels that detect and respond to lung infection, express both receptors, and APN-/- AMs exhibited an inflammatory/M1 phenotype that was associated with decreased fungal killing. Pharmacological stimulation of AMs with AdipoR agonist AdipoRon partially rescued deficient killing in APN-/- AMs that was dependent on both receptors. Finally, APN-enhanced fungal killing was associated with increased activation of the non-canonical LC3 pathway of autophagy. Thus, our study identifies a novel role for APN in LC3-mediated killing of A. fumigatus.

ADIPOQ plays a crucial role in regulating the reproductive system, but there are few reports on the effects of ADIPOQ on ovarian in dairy cows. Previous studies have verified the presence of a 67-bp mutation in the promoter region of the ADIPOQ gene. Hence, we employed ovarian tissues (n = 2111) and blood samples (n = 108) from Chinese Holstein cows as experimental samples to examine the association between ADIPOQ promoter variants and ovarian traits. We extracted DNA from these samples and conducted genetic typing identification on each sample using advanced techniques like PCR and agarose gel electrophoresis. Consequently, the DD, ID, and II genotypes were discovered. and it has been observed that the mutation frequency of this locus is low in the Chinese Holstein cow. Importantly, the correlational analysis unveiled a significant relationship (p < 0.05) between the weight of ovaries in late estrus and the width of ovaries during the estrus interval with the mutation. Result of the RT-PCR revealed that the ID genotype partially diminished the expression of the ADIPOQ gene. The results of this study suggest that the identified variable duplication could serve as a potential genetic marker for enhancing the ovarian traits of Chinese Holstein cows.

Obesity is a prevalent chronic disease that has significant negative impacts on humans and our companion animals, including dogs and cats. Obesity occurs with multiple comorbidities, such as diabetes, hypertension, heart disease and osteoarthritis in dogs and cats. A direct link between lipid metabolism dysregulation and obesity-associated diseases has been implicated. However, the understanding of such pathophysiology in companion animals is limited. This review aims to address the role of lipid metabolism in various metabolic disorders associated with obesity, emphasizing the involvement of the gut microbiota. Furthermore, we also discuss the management of obesity, including approaches like nutritional interventions, thus providing novel insights into obesity prevention and treatment for canines and felines.

The differential diagnosis of lipodystrophy involves other disorders characterized by severe fat loss and may be sometimes challenging. Owing to the rarity of lipodystrophy, it is relevant to search for tools and assays that differentiate it from other diseases that may mimic it. We conducted a study on leptin and high molecular weight (HMW) adiponectin serum concentrations in a series of patients diagnosed with lipodystrophy and compared them with those found in anorexia nervosa, one of the illnesses that may be cause of a missed diagnosis of lipodystrophy.

Leptin and HMW adiponectin serum concentrations were measured in six patients diagnosed with generalized lipodystrophy (GL), six with progeroid syndromes (PS), 13 with familial partial lipodystrophy type 1 (FPLD1, Kobberling syndrome), 10 with familial partial lipodystrophy type 2 (FPLD2, Dunnigan syndrome), 18 with acquired partial lipodystrophy (APL) and 12 affected by anorexia nervosa (AN). Measurements were compared to those obtained in 12 normal weight healthy subjects.

Serum leptin concentrations were reduced to a similar degree in GL, PS and AN, proportionally to the extent of fat loss. Serum concentrations of HMW adiponectin were found extremely low in patients with GL and PS, while comparable to normal weight subjects in patients with AN.

Serum HMW adiponectin can be regarded as a useful tool to discriminate between generalized lipodystrophy syndromes (including PS) and AN.