Notes

We conclude that despite strong associative data, current evidence is inconclusive on the potential causal role of impaired prohormone processing in diabetes and suggest that future work should focus on resolving the question of whether altered prohormone processing is a causal driver or merely a consequence of diabetes pathology
semaglutide results in the Glycemic and Incretin Responses to Intraduodenal Glucose Infusion Between Healthy Young Men and Women.Nutritional Science to Good Health, The University of Adelaide, Adelaide 5000, CONTEXT: Premenopausal women are at a lower risk of type 2 diabetes (T2D) compared to men, but the underlying mechanism(s) remain elusive. The secretion of the incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), from the small intestine is a major determinant of glucose homeostasis and may be influenced by sex.OBJECTIVES: This study compared blood glucose and plasma insulin and incretin responses to intraduodenal glucose infusions in healthy young males and females.DESIGN: In Study 1, 9 women and 20 men received an intraduodenal glucose infusion at 2 kcal/min for 60 minutes. In Study 2, 10 women and 26 men received an intraduodenal glucose at 3 kcal/min for 60 minutes.

Venous blood was sampled every 15 minutes for measurements of blood glucose and plasma insulin, GLP-1 and RESULTS: In response to intraduodenal glucose at 2 kcal/min, the incremental area under the curve between t = 0-60 minutes (iAUC0-60min) for blood glucose and plasma GIP did not differ between the 2 groups. However, iAUC0-60min for plasma GLP-1 (P = 016) and insulin (P = 011) were ∼2-fold higher in women than men. In response to intraduodenal glucose at 3 kcal/min, iAUC0-60min for blood glucose, plasma GIP, and insulin did not differ between women and men, but GLP-1 iAUC0-60min was 2-fold higher in women (P = 012).CONCLUSION: Healthy young women exhibit comparable GIP but a markedly greater GLP-1 response to intraduodenal glucose than men. This disparity warrants further investigations to delineate the underlying mechanisms and may be of relevance to the reduced risk of diabetes in premenopausal women when compared Sepsis-induced activation of endogenous GLP-1 system is enhanced in type 2 to Sackler Medical School Tel Aviv University, Zerifin, Israel.Sackler Medical School Tel Aviv University, Zerifin, Israel.BACKGROUND: High levels of circulating GLP-1 are associated with severity of sepsis in critically ill nondiabetic patients.

Whether glp 1 with type 2 diabetes (T2D) display different activation of the endogenous GLP-1 system during sepsis and whether it is affected by diabetes-related metabolic METHODS: Serum levels of GLP-1 (total and active forms) and its inhibitor enzyme sDPP-4 were determined by ELISA on admission and after 2 to 4 days in 37 sepsis patients with (n = 13) and without T2D (n = 24) and compared to normal healthy controls (n = 25). Correlations between GLP-1 system activation and clinical, inflammatory, and diabetes-related metabolic parameters were performed.RESULTS: A 5-fold (P < 01) and 2-fold (P < 5) increase in active and total GLP-1 levels, respectively, were found on admission as compared to controls. At 2 to 4 days from admission, the level of active GLP-1 forms in surviving patients were decreased significantly (P < 05), and positively correlated with inflammatory marker CRP (r = 03, P = 5). T2D survivors displayed a similar but more enhanced pattern of GLP-1 response than nondiabetic survivors. Nonsurvivors demonstrate an early extreme increase of both total and active GLP-1 forms, 9-fold and 5-fold, respectively (P < 5). The initial and late levels of circulating GLP-1 inhibitory enzyme sDPP-4 were twice lower in all studied groups (P < 01), compared with healthy controls.

CONCLUSIONS: Taken together, these data indicate that endogenous GLP-1 system is activated during sepsis. Patients with T2D display an enhanced and prolonged activation as compared to nondiabetic patients. Extreme early increased GLP-1 levels during sepsis indicate poor prognosis.Enzymatically-Synthesized Glycogen Induces Cecal Glucagon-Like Peptide-1 Production and Suppresses Food Intake in Mice.It is well known that dietary fiber stimulates the release of satiety hormones such as glucagon-like peptide-1 (GLP-1), which in turn suppresses appetite. In order to evaluate appetite regulating role of enzymatically synthesized glycogen (ESG, one of the resistant starch), we examined the effects of dietary supplementation of ESG on food intake and cecal proglucagon gene expression in normal and high fat diet-fed mice. Twenty four male ICR mice were weighed and assigned to four groups: normal diet group; normal diet containing 25% ESG group; high-fat diet (HFD) group; HFD containing 25% ESG group.

Each group was fed the relevant diets for 3 wk. All data were analyzed by a two-way ANOVA with the main effects of HFD and ESG. ESG significantly decreased food intake and increased the weight of the cecum and cecal content. Plasma total short chain fatty acids concentration was significantly elevated by ESG. The mRNA levels of proglucagon in the cecum and plasma total GLP-1 concentration were significantly increased by ESG. The mRNA levels of appetite regulating neuropeptides such as neuropeptide Y, agouti-related protein, proopiomelanocortin, and cocain- and amphetamine-regulating transcript in the hypothalamus were not influenced by ESG.
Here's my website: https://en.wikipedia.org/wiki/Glucagon-like_peptide-1