Residual beta cell function was estimated in 35 young diabetic patients (25 Blacks and 10 Indians) and 22 controls by means of C-peptide assays using glucagon as a provocative agent. The basal C-peptide levels (mean 0,32 +/- 0,23 nmol/l) and the 6-minute post-glucagon levels (mean 0,56 +/- 0,47 nmol/l) were significantly lower in the diabetic patients than in the controls (mean values 0,49 +/- 0,20 nmol/l and 1.24 +/- 0,48 nmol/l respectively). None the less, residual beta cell function, as gauged by the presence of significant C-peptide increments in response to glucagon provocation (mean increase 75% of basal level), was present in most of the patients. The Black patients had significantly lower basal and 6-minute post-glucagon C-peptide levels than the Indian patients.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Real-time detection of somatostatin release from single islets reveals hypersecretion in type 2 diabetes.
Acta Physiol (Oxf)
February 2025
Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
Aim: Somatostatin from pancreatic δ-cells is a paracrine regulator of insulin and glucagon secretion, but the release kinetics and whether secretion is altered in diabetes is unclear. This study aimed to improve understanding of somatostatin secretion by developing a tool for real-time detection of somatostatin release from individual pancreatic islets.
Methods: Reporter cells responding to somatostatin with cytoplasmic Ca concentration ([Ca]) changes were generated by co-expressing somatostatin receptor SSTR2, the G-protein Gα15 and a fluorescent Ca sensor in HeLa cells.
Background: Lipodystrophy encompasses a group of rare disorders associated with severe metabolic disease. These disorders are defined by abnormal fat distribution, with near-total (generalized lipodystrophy, GL) or partial (partial lipodystrophy, PL; i.e.
View Article and Find Full Text PDFAre glucagon-like peptide-1 receptor agonists anti-consummatory drugs?
CNS Spectr
January 2025
Department of Psychiatry, University of Toronto, Toronto, ON, Canada.
Incretin-based treatments, such as glucagon-like peptide-1 receptor (GLP-1R) agonists (eg liraglutide and semaglutide), have rapidly transformed obesity treatment. The well-documented weight loss effect from these agents is considered to be primarily a result of their actions on food intake, but frequent anecdotal reports from varied sources have suggested that they might also broadly affect consummatory behavior, including alcohol and drugs of abuse, suggesting a potential modulatory effect on reward behavior. Herein, we critically review the extant literature on the behavioral effects of GLP-1R agonists in humans, including their impact on feeding behavior, alcohol/drug intake, and overall reward response.
View Article and Find Full Text PDFManaging cardiovascular events, hyperglycemia, and obesity in type 2 diabetes through microRNA regulation linked to glucagon-like peptide-1 receptor agonists.
Diabetol Metab Syndr
January 2025
Department of Medical Laboratory Sciences, School of Allied Medical Sciences, Tehran University of Medical Sciences, Tehran, Iran.
Background And Aims: Type 2 diabetes mellitus (T2DM) is usually complicated by cardiovascular diseases, hyperglycemia, and obesity, which worsen the outcome for the patient. Since recent evidence underlines the epigenetic role of glucagon-like peptide-1 receptor agonists (GLP-1RAs) in the management of these comorbidities, this study compared the effects of these agents, namely liraglutide, semaglutide, dulaglutide, and exenatide, on miRNA regulation in the management of T2DM.
Results: GLP-1RAs modify the expression of miRNAs involved in endothelial function, sugar metabolism, and adipogenesis, including but not limited to miR-27b, miR-130a, and miR-210.
Non-canonical hepatic androgen receptor mediates glucagon sensitivity in female mice through the PGC1α/ERRα/mitochondria axis.
Cell Rep
January 2025
Westlake Laboratory of Life Sciences and Biomedicine, Hangzhou, Zhejiang, China; Key Laboratory of Growth Regulation and Translational Research of Zhejiang Province, School of Life Sciences, Westlake University, Hangzhou, Zhejiang, China; Institute of Basic Medical Sciences, Westlake Institute for Advanced Study, Hangzhou, Zhejiang, China; Research Center for Industries of the Future, Westlake University, Hangzhou, Zhejiang, China. Electronic address:
Glucagon has recently been found to modulate liver fat content, in addition to its role in regulating gluconeogenesis. However, the precise mechanisms by which glucagon signaling synchronizes glucose and lipid metabolism in the liver remain poorly understood. By employing chemical and genetic approaches, we demonstrate that inhibiting the androgen receptor (AR) impairs the ability of glucagon to stimulate gluconeogenesis and lipid catabolism in primary hepatocytes and female mice.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!