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Xi W, Zhao X, Wang B, Zhu Y, Li H. A Review of the Mechanism of Bailing for Diabetic Nephropathy Based on ChatGPT and Network Pharmacology. Int J Clin Pract 2024; 2024. [DOI: 10.1155/2024/1432594] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/15/2023] [Accepted: 07/20/2024] [Indexed: 01/04/2025] Open
Abstract
Diabetes nephropathy (DN) is increasingly recognized as a critical complication in individuals with diabetes and a significant contributor to end‐stage renal disease (ESRD). Bailing capsules, which contain fermented cordyceps mycelium, are commonly utilized in treating various kidney disorders, including DN in clinical practice. This review aims to comprehensively detail the pharmacologically active components of Bailing, its mechanisms of action, and its clinical usage. By employing network pharmacology, we delve into the possible pathways Bailing impacts DN treatment. Current studies suggest that Bailing’s efficacy in DN primarily involves mechanisms related to lipid and atherosclerosis, cancer pathways, and small‐cell lung cancer. Key active ingredients in Bailing that contribute to its therapeutic effects include arachidonic acid, linalyl acetate, β‐sitosterol, and CLR. Furthermore, for literature selection in this review, we integrated GPT‐4 with bias analysis coprocessing. This evaluation provides a foundational understanding and direction for future research into the use of Bailing as a novel treatment for DN.
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Arunachala Murthy T, Chapman M, Jones KL, Horowitz M, Marathe CS. Inter-relationships between gastric emptying and glycaemia: Implications for clinical practice. World J Diabetes 2023; 14:447-459. [PMID: 37273253 PMCID: PMC10236995 DOI: 10.4239/wjd.v14.i5.447] [Citation(s) in RCA: 6] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/24/2022] [Revised: 12/09/2022] [Accepted: 04/07/2023] [Indexed: 05/15/2023] Open
Abstract
Gastric emptying (GE) exhibits a wide inter-individual variation and is a major determinant of postprandial glycaemia in health and diabetes; the rise in blood glucose following oral carbohydrate is greater when GE is relatively more rapid and more sustained when glucose tolerance is impaired. Conversely, GE is influenced by the acute glycaemic environment acute hyperglycaemia slows, while acute hypoglycaemia accelerates it. Delayed GE (gastroparesis) occurs frequently in diabetes and critical illness. In diabetes, this poses challenges for management, particularly in hospitalised individuals and/or those using insulin. In critical illness it compromises the delivery of nutrition and increases the risk of regurgitation and aspiration with consequent lung dysfunction and ventilator dependence. Substantial advances in knowledge relating to GE, which is now recognised as a major determinant of the magnitude of the rise in blood glucose after a meal in both health and diabetes and, the impact of acute glycaemic environment on the rate of GE have been made and the use of gut-based therapies such as glucagon-like peptide-1 receptor agonists, which may profoundly impact GE, in the management of type 2 diabetes, has become commonplace. This necessitates an increased understanding of the complex inter-relationships of GE with glycaemia, its implications in hospitalised patients and the relevance of dysglycaemia and its management, particularly in critical illness. Current approaches to management of gastroparesis to achieve more personalised diabetes care, relevant to clinical practice, is detailed. Further studies focusing on the interactions of medications affecting GE and the glycaemic environment in hospitalised patients, are required.
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Affiliation(s)
- Tejaswini Arunachala Murthy
- Adelaide Medical School, University of Adelaide, Adelaide 5000, SA, Australia
- Intensive Care Unit, Royal Adelaide Hospital, Adelaide 5000, SA, Australia
| | - Marianne Chapman
- Adelaide Medical School, University of Adelaide, Adelaide 5000, SA, Australia
- Intensive Care Unit, Royal Adelaide Hospital, Adelaide 5000, SA, Australia
- NHMRC Centre of Clinical Research Excellence in Nutritional Physiology, Interventions and Outcomes, University of Adelaide, Adelaide 5000, SA, Australia
| | - Karen L Jones
- Adelaide Medical School, University of Adelaide, Adelaide 5000, SA, Australia
- NHMRC Centre of Clinical Research Excellence in Nutritional Physiology, Interventions and Outcomes, University of Adelaide, Adelaide 5000, SA, Australia
| | - Michael Horowitz
- Adelaide Medical School, University of Adelaide, Adelaide 5000, SA, Australia
- NHMRC Centre of Clinical Research Excellence in Nutritional Physiology, Interventions and Outcomes, University of Adelaide, Adelaide 5000, SA, Australia
- Endocrine and Metabolic Unit, Royal Adelaide Hospital, Adelaide 5000, SA, Australia
| | - Chinmay S Marathe
- Adelaide Medical School, University of Adelaide, Adelaide 5000, SA, Australia
- NHMRC Centre of Clinical Research Excellence in Nutritional Physiology, Interventions and Outcomes, University of Adelaide, Adelaide 5000, SA, Australia
- Endocrine and Metabolic Unit, Royal Adelaide Hospital, Adelaide 5000, SA, Australia
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Abstract
This review covers the epidemiology, pathophysiology, clinical features, diagnosis, and management of diabetic gastroparesis, and more broadly diabetic gastroenteropathy, which encompasses all the gastrointestinal manifestations of diabetes mellitus. Up to 50% of patients with type 1 and type 2 DM and suboptimal glycemic control have delayed gastric emptying (GE), which can be documented with scintigraphy, 13C breath tests, or a wireless motility capsule; the remainder have normal or rapid GE. Many patients with delayed GE are asymptomatic; others have dyspepsia (i.e., mild to moderate indigestion, with or without a mild delay in GE) or gastroparesis, which is a syndrome characterized by moderate to severe upper gastrointestinal symptoms and delayed GE that suggest, but are not accompanied by, gastric outlet obstruction. Gastroparesis can markedly impair quality of life, and up to 50% of patients have significant anxiety and/or depression. Often the distinction between dyspepsia and gastroparesis is based on clinical judgement rather than established criteria. Hyperglycemia, autonomic neuropathy, and enteric neuromuscular inflammation and injury are implicated in the pathogenesis of delayed GE. Alternatively, there are limited data to suggest that delayed GE may affect glycemic control. The management of diabetic gastroparesis is guided by the severity of symptoms, the magnitude of delayed GE, and the nutritional status. Initial options include dietary modifications, supplemental oral nutrition, and antiemetic and prokinetic medications. Patients with more severe symptoms may require a venting gastrostomy or jejunostomy and/or gastric electrical stimulation. Promising newer therapeutic approaches include ghrelin receptor agonists and selective 5-hydroxytryptamine receptor agonists.
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Affiliation(s)
- Adil E Bharucha
- Clinical Enteric Neuroscience Translational and Epidemiological Research Program, Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota
| | - Yogish C Kudva
- Division of Endocrinology. Mayo Clinic, Rochester, Minnesota
| | - David O Prichard
- Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota
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Abstract
Gastroparesis is a complication of long-standing type 1 and type 2 diabetes mellitus. Symptoms associated with gastroparesis include early satiety, prolonged postprandial fullness, bloating, nausea and vomiting, and abdominal pain. Mortality is increased in patients with diabetic gastroparesis. A subset of patients with diabetic gastroparesis have pylorospasm that results in obstructive gastroparesis. Current treatment approaches include improving glucose control with insulin and prescribing antinauseant drugs, prokinetic agents, and gastric electric stimulation. Future directions include improved diet counseling based on gastric emptying rate, continuous insulin delivery systems with glucose sensor-augmented monitoring, and drugs for correcting gastric neural and electric abnormalities.
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Affiliation(s)
- Kenneth L Koch
- Section on Gastroenterology, Wake Forest School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157, USA.
| | - Jorge Calles-Escandón
- Section on Endocrinology, MetroHealth Regional, Case Western Reserve University School of Medicine, 2500 Metrohealth Drive, Cleveland, OH 44109, USA
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The ghrelin agonist RM-131 accelerates gastric emptying of solids and reduces symptoms in patients with type 1 diabetes mellitus. Clin Gastroenterol Hepatol 2013; 11:1453-1459.e4. [PMID: 23639598 PMCID: PMC3805699 DOI: 10.1016/j.cgh.2013.04.019] [Citation(s) in RCA: 81] [Impact Index Per Article: 6.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/21/2013] [Revised: 04/02/2013] [Accepted: 04/02/2013] [Indexed: 02/07/2023]
Abstract
BACKGROUND & AIMS RM-131, a synthetic ghrelin agonist, greatly accelerates gastric emptying of solids in patients with type 2 diabetes and delayed gastric emptying (DGE). We investigated the safety and effects of a single dose of RM-131 on gastric emptying and upper gastrointestinal (GI) symptoms in patients with type 1 diabetes and previously documented DGE. METHODS In a double-blind cross-over study, 10 patients with type 1 diabetes (age, 45.7 ± 4.4 y; body mass index, 24.1 ± 1.1 kg/m(2)) and previously documented DGE were assigned in random order to receive a single dose of RM-131 (100 μg, subcutaneously) or placebo. Thirty minutes later, they ate a radiolabeled solid-liquid meal containing EggBeaters (ConAgra Foods, Omaha, NE), and then underwent 4 hours of gastric emptying and 6 hours of colonic filling analyses by scintigraphy. Upper GI symptoms were assessed using a daily diary, gastroparesis cardinal symptom index (total GCSI-DD) and a combination of nausea, vomiting, fullness, and pain (NVFP) scores (each rated on a 0-5 scale). RESULTS At screening, participants' mean level of hemoglobin A1c was 9.1% ± 0.5%; their total GCSI-DD score was 1.66 ± 0.38 (median, 1.71), and their total NVFP score was 1.73 ± 0.39 (median, 1.9). The t1/2 of solid gastric emptying was 84.9 ± 31.6 minutes when subjects were given RM-131 and 118.7 ± 26.7 when they were given a placebo. The median difference (Δ)was 33.9 minutes (interquartile range [IQR] -12, -49), or -54.7% (IQR, -21%,-110%). RM-131 decreased gastric retention of solids at 1 hour (P = .005) and 2 hours (P = .019). Numeric differences in t1/2 for gastric emptying of liquids, solid gastric emptying lag time, and colonic filling at 6 hours were not significant. Total GCSI-DD scores were 0.79 on placebo (IQR, 0.75, 2.08) and 0.17 on RM-131 (IQR, 0.00, 0.67; P = .026); NVFP scores were lower on RM-131 (P = .041). There were no significant adverse effects. CONCLUSIONS RM-131 significantly accelerates gastric emptying of solids and reduces upper GI symptoms in patients with type 1 diabetes and documented DGE.
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Abstract
Severe gastroparesis is a kind of gastroparesis that is refractory to conventional drug therapy and requires nutritional support and frequently emergency hospitalization. The selection of treatment for severe gastroparesis has always been a dilemma for clinicians. Currently, there have been limited reports on the treatment of severe gastroparesis. This article sums up the primary treatments, drug treatments and other kinds of treatments for severe gastroparesis and discusses the prospects for the treatment of this refractory disease.
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Lee AL, Kim CB. The effect of erythromycin on gastrointestinal motility in subtotal gastrectomized patients. JOURNAL OF THE KOREAN SURGICAL SOCIETY 2012; 82:149-55. [PMID: 22403748 PMCID: PMC3294108 DOI: 10.4174/jkss.2012.82.3.149] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 08/30/2011] [Revised: 12/09/2011] [Accepted: 12/16/2011] [Indexed: 01/10/2023]
Abstract
Purpose Our objective was to determine the effect of erythromycin (EM) in improving gastrointestinal motility in subtotal gastrectomized patients. We used radio-opaque Kolomarks as an objective method. We conducted a prospective, controlled clinical trial study of 24 patients. Methods All patients underwent subtotal gastrectomy with 3 capsules containing Kolomarks (20 markers per 1 capsule) in the remnant stomach before anastomosis. From the day of the operation to the 2nd postoperative day, patients in the EM group began receiving 200 mg of EM intravenously for 30 minutes continuously. We counted the number of Kolomarks in the stomach, passed by stomach, in rectum, and in stool with serial simple abdominal X-ray films on the first postoperative day up to the 7th postoperative day. Results The study population included 14 patients in the control group and 10 patients in the EM group. The two study groups were compared in terms of their characteristics including age, gender, past medical history, cancer stage, and operation type. No significant differences were found for the demographics between the two groups. We only found a significant difference for the number of Kolomarks passed by the stomach on the 3rd postoperative day (P = 0.026). Conclusion Our results demonstrated that 200 mg of EM intravenous infusion during the postoperative period induced rapid gastric emptying, although it did not improve gastrointestinal motility for the entire gastrointestinal tract in subtotal gastrectomized patients.
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Affiliation(s)
- A-Lan Lee
- Department of Surgery, Yonsei University College of Medicine, Seoul, Korea
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8
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Abstract
Diabetic gastroparesis (DGP), or slow emptying of the stomach, is a well-established complication of diabetes mellitus and is typically considered to occur in individuals with long-standing type 1 and type 2 diabetes mellitus. Clinical consequences of DGP include induction of gastrointestinal (GI) symptoms (early satiety, abdominal distension, reflux, stomach spasm, postprandial nausea, vomiting), alteration in drug absorption, and destabilization of glycemic control (due to mismatched postprandial glycemic and insulin peaks). Effective nutritional management not only helps in alleviating the symptoms, but also in facilitating better glycemic control. Although there have been no evidence-based guidelines pertaining to the nutrition care process of the DGP, the current dietary recommendations are based on expert opinions or observational studies. The dietary management of gastroparesis needs to be tailored according to the severity of malnutrition and kind of upper GI symptom by changing the volume, consistency, frequency, fiber, fat, and carbohydrates in the meal. Small frequent meals, using more liquid calories, reducing high fat or high fiber, consuming bezoar forming foods, and adjusting meal carbohydrates based on medications or insulin helps in improving the upper GI symptoms and glycemic control. Enteral nutrition can be an option for patients who fail to stabilize their weight loss, or for those who cannot gain weight with oral feedings, while total parenteral nutrition is rarely necessary for the patient with gastroparesis.
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Affiliation(s)
- Amena Sadiya
- Correspondence: Amena Sadiya, Rashid Centre for Diabetes and Research, Ministry of Health, Ajman, United Arab Emirates, Tel +97 167 147 345, Fax +97 167 434 547, Email
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Abstract
Hyperglycemia commonly occurs in acutely ill patients who receive nutrition support, even in patients without a history of diabetes. The traditional view that stress hyperglycemia may be a beneficial adaptive response has been replaced by data linking hyperglycemia with increased morbidity and mortality in critically ill populations. Initial randomized studies to control stress hyperglycemia with intensive insulin infusion reported dramatic decreases in infectious complications and decreased mortality. However, recent large multicenter trials have reported that intensive insulin therapy designed to normalize blood glucose resulted in an unacceptable increase in the incidence of hypoglycemia. Review of the methods, protocols, and nutrition provided during these randomized studies is crucial to understanding the different conclusions reached and how these results may be used to influence protocols in intensive care units today. Evidence is reviewed and practical considerations are provided for nutrition support regimens to minimize stress hypoglycemia and assist glucose management.
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Affiliation(s)
- Joe Krenitsky
- Division of Gastroenterology and Hepatology, University of Virginia Health System, Charlottesville, VA 22908-0673, USA.
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Chang J, Rayner CK, Jones KL, Horowitz M. Diabetic gastroparesis and its impact on glycemia. Endocrinol Metab Clin North Am 2010; 39:745-762. [PMID: 21095542 DOI: 10.1016/j.ecl.2010.08.007] [Citation(s) in RCA: 28] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
Diabetes is the most common cause of gastroparesis and it is now recognized that the relationship between gastric emptying and glycemia is complex and intertwined. Postprandial blood glucose levels influence, and are influenced by, the rate of gastric emptying, highlighting the difficulty in determining which is the cause and which is the effect. Novel diagnostic techniques and therapeutic strategies have been developed for the management of diabetic gastroparesis. This article highlights recent advances in knowledge about diabetic gastroparesis, with an emphasis on the inter-relationships between disordered gastric motor function on glycemia and vice versa, as well as therapeutic strategies for optimizing glycemic control using modulation of gastric emptying.
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Affiliation(s)
- Jessica Chang
- Discipline of Medicine, Royal Adelaide Hospital, University of Adelaide, South Australia 5000, Australia
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11
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Koch KL. Gastric electrical stimulation and the "eye of the beholder". Clin Gastroenterol Hepatol 2010; 8:908-9. [PMID: 20692370 DOI: 10.1016/j.cgh.2010.07.010] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/12/2010] [Accepted: 07/16/2010] [Indexed: 02/07/2023]
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Abstract
We review the current clinical evaluation and management of the most common esophageal and gastrointestinal motility disorders in children based on the literature and our experience in a pediatric motility center in the United States. The disorders discussed include esophageal achalasia, pre- and post-fundoplication motility disorders, gastroparesis, motility disorders occurring after repair of congenital atresias, motility disorders associated with gastroschisis, chronic intestinal pseudo-obstruction, motility after intestinal transplantation, motility disorders after colonic resection for Hirschsprung's disease, chronic functional constipation, and motility disorders associated with imperforate anus.
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Affiliation(s)
- Cheryl E Gariepy
- Center for Cell and Developmental Biology, The Research Institute at Nationwide Children's Hospital, Columbus, Ohio 43205, USA.
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Chapman MJ, Fraser RJL, Matthews G, Russo A, Bellon M, Besanko LK, Jones KL, Butler R, Chatterton B, Horowitz M. Glucose absorption and gastric emptying in critical illness. Crit Care 2009; 13:R140. [PMID: 19712450 PMCID: PMC2750198 DOI: 10.1186/cc8021] [Citation(s) in RCA: 58] [Impact Index Per Article: 3.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/30/2009] [Revised: 08/17/2009] [Accepted: 08/27/2009] [Indexed: 02/07/2023] Open
Abstract
INTRODUCTION Delayed gastric emptying occurs frequently in critically ill patients and has the potential to adversely affect both the rate, and extent, of nutrient absorption. However, there is limited information about nutrient absorption in the critically ill, and the relationship between gastric emptying (GE) and absorption has hitherto not been evaluated. The aim of this study was to quantify glucose absorption and the relationships between GE, glucose absorption and glycaemia in critically ill patients. METHODS Studies were performed in nineteen mechanically-ventilated critically ill patients and compared to nineteen healthy subjects. Following 4 hours fasting, 100 ml of Ensure, 2 g 3-O-methyl glucose (3-OMG) and 99mTc sulphur colloid were infused into the stomach over 5 minutes. Glucose absorption (plasma 3-OMG), blood glucose levels and GE (scintigraphy) were measured over four hours. Data are mean +/- SEM. A P-value < 0.05 was considered significant. RESULTS Absorption of 3-OMG was markedly reduced in patients (AUC240: 26.2 +/- 18.4 vs. 66.6 +/- 16.8; P < 0.001; peak: 0.17 +/- 0.12 vs. 0.37 +/- 0.098 mMol/l; P < 0.001; time to peak; 151 +/- 84 vs. 89 +/- 33 minutes; P = 0.007); and both the baseline (8.0 +/- 2.1 vs. 5.6 +/- 0.23 mMol/l; P < 0.001) and peak (10.0 +/- 2.2 vs. 7.7 +/- 0.2 mMol/l; P < 0.001) blood glucose levels were higher in patients; compared to healthy subjects. In patients; 3-OMG absorption was directly related to GE (AUC240; r = -0.77 to -0.87; P < 0.001; peak concentrations; r = -0.75 to -0.81; P = 0.001; time to peak; r = 0.89-0.94; P < 0.001); but when GE was normal (percent retention240 < 10%; n = 9) absorption was still impaired. GE was inversely related to baseline blood glucose, such that elevated levels were associated with slower GE (ret 60, 180 and 240 minutes: r > 0.51; P < 0.05). CONCLUSIONS In critically ill patients; (i) the rate and extent of glucose absorption are markedly reduced; (ii) GE is a major determinant of the rate of absorption, but does not fully account for the extent of impaired absorption; (iii) blood glucose concentration could be one of a number of factors affecting GE.
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Affiliation(s)
- Marianne J Chapman
- Department of Anaesthesia and Intensive Care, Royal Adelaide Hospital, North Terrace, Adelaide, SA 5000, Australia
- School of Medicine, University of Adelaide, Adelaide, SA 5000, Australia
| | - Robert JL Fraser
- School of Medicine, University of Adelaide, Adelaide, SA 5000, Australia
- Investigation & Procedures Unit, Repatriation General Hospital, Daws Road, Daw Park, SA 5041, Australia
| | - Geoffrey Matthews
- Centre for Paediatric and Adolescent Gastroenterology, Women's and Children's Hospital; 72 King William Road, Adelaide, SA 5006, Australia
| | - Antonietta Russo
- School of Medicine, University of Adelaide, Adelaide, SA 5000, Australia
| | - Max Bellon
- Department of Nuclear Medicine, Royal Adelaide Hospital, North Terrace, Adelaide, SA 5000, Australia
| | - Laura K Besanko
- Investigation & Procedures Unit, Repatriation General Hospital, Daws Road, Daw Park, SA 5041, Australia
| | - Karen L Jones
- School of Medicine, University of Adelaide, Adelaide, SA 5000, Australia
| | - Ross Butler
- Centre for Paediatric and Adolescent Gastroenterology, Women's and Children's Hospital; 72 King William Road, Adelaide, SA 5006, Australia
| | - Barry Chatterton
- Department of Nuclear Medicine, Royal Adelaide Hospital, North Terrace, Adelaide, SA 5000, Australia
| | - Michael Horowitz
- School of Medicine, University of Adelaide, Adelaide, SA 5000, Australia
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Khoo J, Rayner CK, Jones KL, Horowitz M. Pathophysiology and management of gastroparesis. Expert Rev Gastroenterol Hepatol 2009; 3:167-181. [PMID: 19351287 DOI: 10.1586/egh.09.10] [Citation(s) in RCA: 20] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
Gastroparesis is characterized by upper gastrointestinal symptoms associated with delayed gastric emptying, without mechanical obstruction. However, symptoms do not correlate well with the magnitude of delay in gastric emptying. Diabetes mellitus and surgery are the most common causes, although more than 30% of cases are idiopathic. Coordination of insulin action with nutrient delivery is important in diabetics, as postprandial blood glucose levels and gastric emptying are interdependent, and gastroparesis probably represents a major cause of poor glycemic control. Scintigraphy is the gold standard for measuring gastric emptying. Current treatment mainly involves the use of prokinetic drugs. Pyloric botulinum toxin injection and gastric electrical stimulation require more evidence from controlled studies before their use can be recommended. Surgical options remain inadequately studied.
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Affiliation(s)
- Joan Khoo
- Discipline of Medicine, University of Adelaide, Royal Adelaide Hospital, South Australia, Australia
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Bradshaw LA, Sims JA, Richards WO. Noninvasive assessment of the effects of glucagon on the gastric slow wave. Am J Physiol Gastrointest Liver Physiol 2007; 293:G1029-38. [PMID: 17884978 PMCID: PMC2726773 DOI: 10.1152/ajpgi.00054.2007] [Citation(s) in RCA: 12] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/31/2023]
Abstract
Hyperglycemic effects on the gastric slow wave are not well understood, and no studies have examined the effects that hyperglycemia has on gastric slow wave magnetic fields. We recorded multichannel magnetogastrograms (MGGs) before and after intravenous administration of glucagon and subsequent modest hyperglycemia in 20 normal volunteers. Normal slow waves were evident in baseline MGG recordings from all 20 subjects, but within 15 min after glucagon had been given, we noted significant effects on MGG signals. In addition to an overall decrease in the slow wave frequency from 2.9 +/- 0.5 cycles per min (cpm) to 2.2 +/- 0.1 cpm (P < 0.05), we observed significant changes in the number and range of spectral peaks recorded. Furthermore, the propagation velocity determined from surface current density maps computed from the multichannel MGG decreased significantly (7.1 +/- 0.8 mm/s to 5.0 +/- 0.3 mm/s, P < 0.05). This is the first study of biomagnetic effects of hyperglycemia in normal subjects. Our results suggest that the analysis of the MGG provides parameter quantification for gastric electrical activity specific to and characteristic of slow wave abnormalities associated with increased serum glucose by injection of glucagon.
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Affiliation(s)
- L Alan Bradshaw
- Department of Surgery, Vanderbilt University, Nashville, TN, USA.
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Kwiatek MA, Steingoetter A, Pal A, Menne D, Brasseur JG, Hebbard GS, Boesiger P, Thumshirn M, Fried M, Schwizer W. Quantification of distal antral contractile motility in healthy human stomach with magnetic resonance imaging. J Magn Reson Imaging 2007; 24:1101-9. [PMID: 17031837 DOI: 10.1002/jmri.20738] [Citation(s) in RCA: 71] [Impact Index Per Article: 3.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/15/2022] Open
Abstract
PURPOSE To quantify healthy postprandial: 1) propagation, periodicity, geometry, and percentage occlusion by distal antral contraction waves (ACWs); and 2) changes in ACW activity in relationship to gastric emptying (GE). MATERIALS AND METHODS Using 1.5-T MR scanner, nine healthy fasted volunteers were examined in the right decubitus position after ingestion of 500 mL of 10% glucose (200 kcal) with 500 microM Gd-DOTA. Total gastric (TGV) and meal volumes (MV) were assessed every five minutes for 90 minutes, in and interspersed with dynamic scan sequences (duration: 2.78 minutes) providing detailed images of distal ACWs. RESULTS TGV increased by 738+/-38 mL after ingestion (t0), subsequently decreasing in parallel to GE. The mean GE rate and half-emptying time were 24+/-3 mL/5 minutes and 71+/-6 minutes, respectively. Accompanying ACWs reached a periodicity of 23+/-2 seconds at t35 and propagated at an unvarying speed of 0.27+/-0.01 cm/second. Their amplitude of 0.70+/-0.08 cm was constant, but the width decreased along the antral wall by 6+/-2%/cm (P=0.003). ACWs were nonocclusive (percentage occlusion 58.1+/-5.9%, t0 at the pylorus) with a reduction in occlusion away from the pylorus (P<0.001). No propagation and geometry characteristics of ACWs correlated with the changes of MV (mL/5 minutes; R2<0.05). CONCLUSION Our results indicate that ACWs are not imperative for emptying of liquids. This study provides a detailed quantitative reference for MRI inquiries into pharmacologically- and pathologically-altered gastric motility.
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Affiliation(s)
- Monika A Kwiatek
- Division of Gastroenterology and Hepatology, University Hospital Zurich, Zurich, Switzerland.
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Chaikomin R, Rayner CK, Jones KL, Horowitz M. Upper gastrointestinal function and glycemic control in diabetes mellitus. World J Gastroenterol 2006; 12:5611-5621. [PMID: 17007012 PMCID: PMC4088160 DOI: 10.3748/wjg.v12.i35.5611] [Citation(s) in RCA: 28] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/19/2006] [Revised: 06/06/2006] [Accepted: 06/16/2006] [Indexed: 02/06/2023] Open
Abstract
Recent evidence has highlighted the impact of glycemic control on the incidence and progression of diabetic micro- and macrovascular complications, and on cardiovascular risk in the non-diabetic population. Postprandial blood glucose concentrations make a major contribution to overall glycemic control, and are determined in part by upper gastrointestinal function. Conversely, poor glycemic control has an acute, reversible effect on gastrointestinal motility. Insights into the mechanisms by which the gut contributes to glycemia have given rise to a number of novel dietary and pharmacological strategies designed to lower postprandial blood glucose concentrations.
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Affiliation(s)
- Reawika Chaikomin
- Department of Medicine, Royal Adelaide Hospital, North Terrace, Adelaide, South Australia 5000, Australia
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Lacy BE, Crowell MD, Schettler-Duncan A, Mathis C, Pasricha PJ. The treatment of diabetic gastroparesis with botulinum toxin injection of the pylorus. Diabetes Care 2004; 27:2341-7. [PMID: 15451898 DOI: 10.2337/diacare.27.10.2341] [Citation(s) in RCA: 90] [Impact Index Per Article: 4.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/03/2023]
Abstract
OBJECTIVE Gastroparesis is a disorder of delayed gastric emptying that is often chronic in nature. Up to 50% of type 1 diabetic subjects have symptoms of gastroparesis, which include nausea, vomiting, and early satiety. Elevated pyloric pressures may be responsible for delayed gastric emptying in diabetic subjects. Botulinum toxin inhibits the release of acetylcholine and produces transient paralysis when injected into smooth muscle. The aim of this study was to determine whether injection of the pylorus with botulinum toxin in patients with diabetic gastroparesis improves symptoms of gastroparesis, alters gastric emptying scan time, and/or changes weight and insulin use. RESEARCH DESIGN AND METHODS This was an open-label trial with age- and sex-matched control subjects from a tertiary care referral center for patients with gastroparesis. Eight type 1 diabetic subjects (six women and two men; mean age 41 years; mean years with diabetes 25.3) who had failed standard therapy were enrolled. Intervention consisted of injection of the pylorus with 200 units of botulinum toxin during upper endoscopy. Symptoms, antropyloric manometry, gastric emptying scan times, weight, and insulin use were all recorded before intervention and during a 12-week follow-up period. RESULTS Seven of the eight patients completed the full 12-week follow-up period. No complications were noted. Mean symptom scores declined from 27 to 12.1 (P < 0.01), whereas the SF-36 physical functioning domain also improved (P < 0.05). Four patients noted an increase in insulin use of >5 units/day. Six of the seven patients gained weight (P = 0.05). Gastric emptying scan time improved in four patients. CONCLUSIONS Botulinum toxin injection of the pylorus is safe and improves symptoms in patients with diabetic gastroparesis. These results warrant further investigation with a large, double-blind, placebo-controlled trial.
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Affiliation(s)
- Brian E Lacy
- Marvin M. Schuster Center for Digestive and Motility Disorders, Johns Hopkins University, School of Medicine, Baltimore, MD, USA.
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Russo A, Stevens JE, Giles N, Krause G, O'Donovan DG, Horowitz M, Jones KL. Effect of the motilin agonist KC 11458 on gastric emptying in diabetic gastroparesis. Aliment Pharmacol Ther 2004; 20:333-338. [PMID: 15274670 DOI: 10.1111/j.1365-2036.2004.02066.x] [Citation(s) in RCA: 36] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
BACKGROUND KC 11458, a motilin agonist without antibiotic properties, accelerates gastric emptying in animals and healthy humans. AIM To evaluate the acute effects of KC 11458 on gastric emptying in diabetic gastroparesis. METHODS Twenty-nine patients (6 type 1 and 23 type 2) with gastroparesis underwent assessments of: (i) gastric emptying of a solid/liquid meal using scintigraphy, (ii) glycaemic control (blood glucose at 0, 30, 60, 90 and 120 min during the gastric emptying measurement) and (iii) upper gastrointestinal and 'meal-related' symptoms (questionnaire), at baseline and after treatment with KC 11458 in a dose of 8 mg t.d.s., or placebo for 8 days. RESULTS KC 11458 had no statistically significant or clinically relevant effect on gastric emptying of either the solid intragastric retention at 100 min (T100) (P = 0.87) or liquid 50% emptying time (T50) (P = 0.17) components of the meal. KC 11458 slightly worsened (P = 0.04) upper gastrointestinal symptoms when compared with placebo. The magnitude of the change in solid gastric emptying correlated with the change in the blood glucose concentration (r = 0.49; P < 0.05). CONCLUSIONS KC 11458, in a dose of 8 mg t.d.s. for 8 days, does not accelerate gastric emptying in patients with diabetic gastroparesis. The absence of efficacy may relate to an effect of hyperglycaemia.
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Affiliation(s)
- A Russo
- Department of Medicine, Royal Adelaide Hospital, University of Adelaide, Australia
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Jones KL, Russo A, Stevens JE, Wishart JM, Berry MK, Horowitz M. Predictors of delayed gastric emptying in diabetes. Diabetes Care 2001; 24:1264-1269. [PMID: 11423513 DOI: 10.2337/diacare.24.7.1264] [Citation(s) in RCA: 217] [Impact Index Per Article: 9.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
OBJECTIVE To define the predictors of the rate of gastric emptying in patients with diabetes. RESEARCH DESIGN AND METHODS A total of 101 outpatients with diabetes (79 type 1 and 22 type 2) underwent measurements of gastric emptying of a solid/liquid meal (scintigraphy), upper gastrointestinal symptoms (questionnaire), glycemic control (blood glucose concentrations during gastric emptying measurement), and autonomic nerve function (cardiovascular reflexes). RESULTS The gastric emptying of solid and/or liquid was delayed in 66 (65%) patients. Solid (retention at 100 min 64 +/- 3.2 vs. 50.2 +/- 3.6%, P < 0.005) and liquid (retention at 100 min 22.7 +/- 1.7 vs. 16.0 +/- 1.8%, P < 0.001) gastric emptying was slower in women than in men. Of all upper gastrointestinal symptoms (including nausea and vomiting), only abdominal bloating/fullness was associated with slower gastric emptying (P < 0.005). A multiple regression analysis demonstrated that both abdominal bloating/fullness and female sex were predictors of slower gastric emptying of both solids and liquids. CONCLUSIONS We conclude that the presence of abdominal bloating/fullness but not any other upper gastrointestinal symptom is associated with diabetic gastroparesis and that gastric emptying is slower in diabetic women than in diabetic men.
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Affiliation(s)
- K L Jones
- Department of Medicine, University of Adelaide, Royal Adelaide Hospital, Adelaide, Australia.
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Rayner CK, Samsom M, Jones KL, Horowitz M. Relationships of upper gastrointestinal motor and sensory function with glycemic control. Diabetes Care 2001; 24:371-381. [PMID: 11213895 DOI: 10.2337/diacare.24.2.371] [Citation(s) in RCA: 305] [Impact Index Per Article: 12.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
Acute changes in the blood glucose concentration have a major reversible effect on esophageal, gastric, intestinal, gallbladder, and anorectal motility in both healthy subjects and diabetic patients. For example, gastric emptying is slower during hyperglycemia than euglycemia and accelerated during hypoglycemia. Acute hyperglycemia also affects perceptions arising from the gastrointestinal tract and may accordingly, be important in the etiology of gastrointestinal symptoms in diabetes. Elevations in blood glucose that are within the normal postprandial range also affect gastrointestinal motor and sensory function. Upper gastrointestinal motor function is a critical determinant of postprandial blood glucose concentrations by influencing the absorption of ingested nutrients. Interventions that reduce postprandial hyperglycemia, by modulating the rate of gastric emptying, have the potential to become mainstream therapies in the treatment of diabetes.
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Affiliation(s)
- C K Rayner
- University of Adelaide Department of Medicine, Royal Adelaide Hospital, South Australia, Australia
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