scholarly journals Glucagon-like peptide-1 and beta cell glucose sensitivity-a glucose ramp study in mice

Peptides ◽  
2021 ◽  
pp. 170650
Author(s):  
Bo Ahrén
Keyword(s):  
Beta Cell ◽  
Beta Cell Glucose Sensitivity ◽  
Glucose Sensitivity ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Cell Glucose

scholarly journals Genome-Wide Association Analysis of Pancreatic Beta-Cell Glucose Sensitivity

2020 ◽  
Vol 106 (1) ◽  
pp. 80-90
Author(s):  
Harshal A Deshmukh ◽  
Anne Lundager Madsen ◽  
Ana Viñuela ◽  
Christian Theil Have ◽  
Niels Grarup ◽  
...  
Keyword(s):  
Beta Cell ◽  
Meta Analysis ◽  
Pancreatic Beta Cell ◽  
P Value ◽  
Genetic Determinants ◽  
Genome Wide ◽  
Beta Cell Glucose Sensitivity ◽  
Glucose Sensitivity ◽  
Cell Glucose

Abstract Context Pancreatic beta-cell glucose sensitivity is the slope of the plasma glucose-insulin secretion relationship and is a key predictor of deteriorating glucose tolerance and development of type 2 diabetes. However, there are no large-scale studies looking at the genetic determinants of beta-cell glucose sensitivity. Objective To understand the genetic determinants of pancreatic beta-cell glucose sensitivity using genome-wide meta-analysis and candidate gene studies. Design We performed a genome-wide meta-analysis for beta-cell glucose sensitivity in subjects with type 2 diabetes and nondiabetic subjects from 6 independent cohorts (n = 5706). Beta-cell glucose sensitivity was calculated from mixed meal and oral glucose tolerance tests, and its associations between known glycemia-related single nucleotide polymorphisms (SNPs) and genome-wide association study (GWAS) SNPs were estimated using linear regression models. Results Beta-cell glucose sensitivity was moderately heritable (h2 ranged from 34% to 55%) using SNP and family-based analyses. GWAS meta-analysis identified multiple correlated SNPs in the CDKAL1 gene and GIPR-QPCTL gene loci that reached genome-wide significance, with SNP rs2238691 in GIPR-QPCTL (P value = 2.64 × 10−9) and rs9368219 in the CDKAL1 (P value = 3.15 × 10−9) showing the strongest association with beta-cell glucose sensitivity. These loci surpassed genome-wide significance when the GWAS meta-analysis was repeated after exclusion of the diabetic subjects. After correction for multiple testing, glycemia-associated SNPs in or near the HHEX and IGF2B2 loci were also associated with beta-cell glucose sensitivity. Conclusion We show that, variation at the GIPR-QPCTL and CDKAL1 loci are key determinants of pancreatic beta-cell glucose sensitivity.

scholarly journals Impaired beta cell glucose sensitivity and whole-body insulin sensitivity as predictors of hyperglycaemia in non-diabetic subjects

Diabetologia ◽  
2005 ◽  
Vol 48 (12) ◽  
pp. 2470-2476 ◽  
Author(s):  
M. Walker ◽  
A. Mari ◽  
M. K. Jayapaul ◽  
S. M. A. Bennett ◽  
E. Ferrannini
Keyword(s):  
Insulin Sensitivity ◽  
Beta Cell ◽  
Whole Body ◽  
Beta Cell Glucose Sensitivity ◽  
Glucose Sensitivity ◽  
Cell Glucose

scholarly journals Acute Effects of Dietary Carbohydrate Restriction on Glycemia, Lipemia and Appetite Regulating Hormones in Normal-Weight to Obese Subjects

Nutrients ◽  
2018 ◽  
Vol 10 (9) ◽  
pp. 1285 ◽  
Author(s):  
Amirsalar Samkani ◽  
Mads Skytte ◽  
Mads Thomsen ◽  
Arne Astrup ◽  
Carolyn Deacon ◽  
...  
Keyword(s):  
Beta Cell ◽  
Gut Hormones ◽  
Normal Weight ◽  
Metabolic Effects ◽  
Dietary Carbohydrate ◽  
Acute Effects ◽  
Postprandial Glycemia ◽  
Beta Cell Glucose Sensitivity ◽  
Glucose Sensitivity ◽  
Cell Glucose

Postprandial responses to food are highly dependent on the macronutrient composition of the diet. We investigated the acute effects of transition from the recommended moderately high carbohydrate (HC) diet towards a carbohydrate-reduced high-protein (CRHP) diet on postprandial glycemia, insulinemia, lipemia, and appetite-regulating hormones in non-diabetic adults. Fourteen subjects, including five males (Mean ± SD: age 62 ± 6.5; BMI 32 ± 7.6 kg/m2; hemoglobin A1c (HbA1c) 40 ± 3.0 mmol/mol; HOMA2-IR 2.1 ± 0.9) were included in this randomized, cross-over study. Iso-caloric diets were consumed for two consecutive days with a median wash-out period of 21 days (range 2–8 weeks) between diets (macronutrient energy composition: CRHP/HC; 31%/54% carbohydrate, 29%/16% protein, 40%/30% fat). Postprandial glucose, insulin secretion rate (ISR), triglycerides (TGs), non-esterified fatty acids (NEFAs), and satiety ratings were assessed after ingestion of breakfast (Br) and lunch (Lu), and gut hormones and glucagon were assessed after ingestion of Br. Compared with the HC diet, the CRHP diet reduced peak glucose concentrations (Br 11%, p = 0.024; Lu 11%, p < 0.001), glucose excursions (Br 80%, p = 0.20; Lu 85%, p < 0.001), and ISR (Br 31%; Lu 64%, both p < 0.001) whereas CRHP, as compared with HC, increased glucagon-like peptide-1 (Br 27%, p = 0.015) and glucagon values (Br 249%, p < 0.001). NEFA and TG levels increased in the CRHP diet as compared with the HC diet after Br, but no difference was found after Lu (NEFA Br 22%, p < 0.01; TG Br 42%, p = 0.012). Beta-cell glucose sensitivity, insulin clearance, cholecystokinin values, and subjective satiety ratings were unaffected. It is possible to achieve a reduction in postprandial glycemia and insulin without a deleterious effect on beta-cell glucose sensitivity by substituting part of dietary carbohydrate with iso-caloric protein and fat in subjects without type 2 diabetes mellitus (T2DM). The metabolic effects are more pronounced after the second meal.

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