Interactions between the heart and other organs have been a focus in acute decompensated heart failure (ADHF). However, the association between ADHF and pancreatic exocrine insufficiency (PEI), which may lead to malnutrition, remains unclear. We investigated the relationship between exocrine pancreatic enzymes and ADHF.

We enrolled 155 and 46 patients with and without ADHF, respectively. Serum amylase and lipase levels were compared between the two groups. In the ADHF group, factors correlating with serum amylase or lipase levels were assessed using multiple regression analysis, and changes in their levels throughout the hospital course were determined.

Patients with ADHF exhibited significantly lower amylase and lipase levels. In the same group, the significant independent correlates of lower amylase levels included a lower blood urea-nitrogen level (partial correlation coefficient, 0.530; p < 0.001), lower albumin level (partial correlation coefficient, 0.252; p = 0.015), and higher uric acid level (partial correlation coefficient, -0.371; p < 0.001). The significant independent correlates of lower lipase levels included coexisting atrial fibrillation (coefficient, 0.287; p = 0.026), lower creatinine level (coefficient, 0.236; p = 0.042), and higher B-type natriuretic peptide level (coefficient, -0.257; p = 0.013). Both amylase and lipase levels significantly increased following the improvement in ADHF.

In patients with ADHF, decreased serum amylase and lipase levels were associated with the congestion severity, suggesting that PEI may occur in patients with ADHF, potentially due to ADHF-related congestion.

Multiple factors, such as dietary patterns, pharmaceutical interventions, and exposure to harmful substances, possess the capacity to influence gut microbiota composition. Gut microbiota dysbiosis has emerged as a significant contributor to the progression of chronic kidney disease (CKD) and its associated complications. By comprehending the intricacies of the intestinal microbiota, this research endeavor holds the potential to offer novel perspectives on potential strategies for mitigating CKD progression.

In this retrospective analysis, we assessed gut microbiota composition in CKD patients. Fecal samples were collected from a cohort of 44 patients with stage 3-4 CKD, alongside a control group consisting of 132 healthy volunteers. Subsequently, 16 s rDNA sequencing was conducted to examine the composition of the gut microbiota.

Our findings revealed significant alterations in the diversity of intestinal microbiota in fecal samples between patients with stage 3-4 CKD and healthy subjects. Among the 475 bacterial genera, 164 were shared, while 242 dominant genera were exclusive to healthy subjects and 69 to CKD stages 3-4 samples. Notably, healthy volunteers exhibited a prevalence of intestinal Firmicutes and Bacteroidetes, whereas stage 3-4 CKD patients displayed higher abundance of Proteobacteria and Actinobacteria. The presence of uncultured Coprobacillus sp. notably contributed to distinguishing between the two groups. ROC curve analysis identified distinct microbiota with superior diagnostic efficacy for discriminating stage 3-4 CKD patients from healthy individuals. Metabolic pathway analysis revealed differing dominant pathways between the two groups-the NADH dehydrogenase pathway in healthy individuals and the phosphate acetyltransferase pathway in stage 3-4 CKD patients. Moreover, the CKD cohort displayed a higher proportion of Gram-negative bacteria and facultative anaerobes.

In conclusion, our study underscores the profound influence of gut microbiota dysbiosis on CKD progression. The distinct microbial profiles observed in CKD patients highlight the potential efficacy of microbiota-based interventions in mitigating CKD advancement.

Black American mink (Neovison vison), which had been selected for tolerance to Aleutian mink disease virus (AMDV) for more than 20 years (TG100) or were from herds that have been free of AMDV (TG0), along with their progeny and crosses with 50% and 75% tolerance ancestry, were inoculated with a local isolate of AMDV. Blood samples were collected from 493 mink between 120 and 1211 days post-inoculation, and concentrations of 14 serum analytes were measured. Distributions of all analytes significantly deviated from normality, and data were analyzed after Box-Cox power transformation. Significant differences were observed among tolerant groups in the concentrations of globulin (GLO), total protein (TP), alkaline phosphatase, urea nitrogen, and calcium. Concentrations of GLO and TP linearly and significantly decreased with an increasing percentage of tolerance ancestry. Eleven analytes had the smallest values in the tolerant groups (TG100 or TG75), and eight analytes had the greatest values in the non-selected groups (TG0 or TG50). Antibody titer had the greatest correlation coefficients with GLO (0.62), TP (0.53), and creatinine (0.36). It was concluded that selection for tolerance decreased the concentrations of most serum analytes, and TP and GLO were the most accurate biomarkers of tolerance to AMDV infection. Males had significantly greater values than females for phosphorus and total bilirubin concentrations, but females had significantly greater amylase, cholesterol, and BUN concentrations than males.

While there is plentiful evidence on elevated serum levels of amylase, lipase, and trypsin in acute illness, low serum levels of these digestive enzymes have been studied infrequently. The aim was to systematically review published studies on the relationship between low serum levels of amylase, lipase, or trypsin and metabolic disorders.

The search was conducted in MEDLINE and Scopus databases. Studies in humans were included if they reported on the association between serum levels of amylase, lipase, or trypsin within normal range and metabolic disorders. Random-effects meta-analysis was conducted.

A total of 20 studies encompassing 20,916 participants were included. Compared with healthy individuals, individuals with type 2 diabetes mellitus (mean difference = -5.3; p < 0.001), metabolic syndrome (mean difference = -5.1; p < 0.001), and overweight/obesity (mean difference = -0.8; p = 0.02) had significantly lower serum levels of amylase. Both individuals with type 1 diabetes mellitus (mean difference = -1.8; p < 0.001) and type 2 diabetes mellitus (mean difference = -0.8; p < 0.001) had significantly lower serum levels of lipase compared with healthy individuals. Data on serum trypsin were not suitable for meta-analysis. In the pooled analysis, individuals with type 2 diabetes mellitus had 3.1-times lower serum levels of amylase, 2.9-times lower serum levels of lipase, and 2.5-times lower serum levels of trypsin levels than the upper limits of normal for the three digestive enzymes.

Low serum levels of amylase and lipase are significantly associated with type 2 diabetes mellitus, type 1 diabetes mellitus, excess adiposity, and metabolic syndrome. The role of digestive enzymes in the pathogenesis of metabolic disorders warrants further investigations.

Sepsis is a major cause of mortality among critically ill patients in the intensive care unit (ICU). Alterations in serum amyloid A (SAA) and nitric oxide (NO) levels have been associated with mortality in critically ill patients. In the present study, we investigated the predictive value of SAA and/or NO compared to traditional predictive markers such as C-reactive protein (CRP) and Acute Physiology and Chronic Health Evaluation II (APACHE II) score.

100 adult patients with sepsis and 25 without sepsis were enrolled in a prospective, randomized study in our ICU. The APACHE II score was calculated, and their peripheral venous blood SAA, NO and CRP levels were evaluated on days 1, 3, and 7 after sepsis was diagnosed. The patients were sorted based on incidence of septic shock into septic shock (A) and non-septic shock (B) groups. Comparative analyses of altered levels of these indicators between the two groups were performed, and correlations between SAA, NO, and the more traditional APACHE II score were probed. Patients were sorted based on survival status into death (D) and survival (S) groups based on death endpoint within 28 days after admission.

We observed that the difference in APACHE II score, SAA and CRP levels were statistically significantly (p < 0.05) between groups A and B on days 1, 3 and 7 post-diagnosis, while inter-group NO level significantly differed (p < 0.05) on days 1 and 3 post-diagnosis, no apparent difference was observed on day 7 post-diagnosis. For groups D and S, SAA, CRP and NO levels significantly differed (p < 0.05) on days 3 and 7 post-diagnosis, with no apparent difference on day 1. APACHE II score was significantly different on day 7 (p < 0.05), however the difference on days 1 and 3 were non-significant. We also demonstrated a positive correlation between APACHE II scores, SAA levels on days 1, 3, and 7, as well as NO levels on days 1 and 3. In addition, for the D and S groups, SAA at all time points, NO on day 3 and CRP on day 7 positively correlated with increased death events.

The dynamic monitoring of SAA and NO serum levels with APACHE II scores better reflect the severity of sepsis than traditional indicators like CRP and may serve as independent prognosticators of sepsis in critically ill patients, shorten time to diagnosis confirmation and improve therapeutic decision-making.

For the last decade, low serum amylase (hypoamylasemia) has been reported in certain common cardiometabolic conditions such as obesity, diabetes (regardless of type), and metabolic syndrome, all of which appear to have a common etiology of insufficient insulin action due to insulin resistance and/or diminished insulin secretion. Some clinical studies have shown that salivary amylase may be preferentially decreased in obese individuals, whereas others have revealed that pancreatic amylase may be preferentially decreased in diabetic subjects with insulin dependence. Despite this accumulated evidence, the clinical relevance of serum, salivary, and pancreatic amylase and the underlying mechanisms have not been fully elucidated. In recent years, copy number variations (CNVs) in the salivary amylase gene (AMY1), which range more broadly than the pancreatic amylase gene (AMY2A and AMY2B), have been shown to be well correlated with salivary and serum amylase levels. In addition, low CNV of AMY1, indicating low salivary amylase, was associated with insulin resistance, obesity, low taste perception/satiety, and postprandial hyperglycemia through impaired insulin secretion at early cephalic phase. In most populations, insulin-dependent diabetes is less prevalent (minor contribution) compared with insulin-independent diabetes, and obesity is highly prevalent compared with low body weight. Therefore, obesity as a condition that elicits cardiometabolic diseases relating to insulin resistance (major contribution) may be a common determinant for low serum amylase in a general population. In this review, the novel interpretation of low serum, salivary, and pancreas amylase is discussed in terms of major contributions of obesity, diabetes, and metabolic syndrome.

To identify metabolic pathways that are perturbed in pancreatic ductal adenocarcinoma (PDAC), we investigated gene-metabolite networks with integration of metabolomics and transcriptomics.

We conducted global metabolite profiling analysis on two independent cohorts of resected PDAC cases to identify critical metabolites alteration that may contribute to the progression of pancreatic cancer. We then searched for gene surrogates that were significantly correlated with the key metabolites, by integrating metabolite and gene expression profiles.

Fifty-five metabolites were consistently altered in tumors as compared with adjacent nontumor tissues in a test cohort (N = 33) and an independent validation cohort (N = 31). Weighted network analysis revealed a unique set of free fatty acids (FFA) that were highly coregulated and decreased in PDAC. Pathway analysis of 157 differentially expressed gene surrogates revealed a significantly altered lipid metabolism network, including key lipolytic enzymes PNLIP, CLPS, PNLIPRP1, and PNLIPRP2. Gene expressions of these lipases were significantly decreased in pancreatic tumors as compared with nontumor tissues, leading to reduced FFAs. More importantly, a lower gene expression of PNLIP in tumors was associated with poorer survival in two independent cohorts. We further showed that two saturated FFAs, palmitate and stearate, significantly induced TRAIL expression, triggered apoptosis, and inhibited proliferation in pancreatic cancer cells.

Our results suggest that impairment in a lipolytic pathway involving lipases, and a unique set of FFAs, may play an important role in the development and progression of pancreatic cancer and provide potential targets for therapeutic intervention.