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Effects of carbohydrate restriction on postprandial glucose metabolism, β-cell function, gut hormone secretion, and satiety in patients with Type 2 diabetes.

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Dietary carbohydrate restriction may improve the phenotype of Type 2 diabetes (T2D) patients. We aimed to investigate 6 wk of carbohydrate restriction on postprandial glucose metabolism, pancreatic α- and β-cell function, gut hormone secretion, and satiety in T2D patients. Methods In a crossover design, 28 T2D patients (mean HbA 1c: 60 mmol/mol) were randomized to 6 wk of carbohydrate-reduced high-protein (CRHP) diet and 6 wk of conventional diabetes (CD) diet (energy-percentage carbohydrate/protein/fat: 30/30/40 vs. 50/17/33). Twenty-four-hour continuous glucose monitoring (CGM) and mixed-meal tests were undertaken and fasting intact proinsulin (IP), 32,33 split proinsulin concentrations (SP), and postprandial insulin secretion rates (ISR), insulinogenic index (IGI), β-cell sensitivity to glucose ( B up), glucagon, and gut hormones were measured. Gastric emptying was evaluated by postprandial paracetamol concentrations and satiety by visual analog scale ratings. A CRHP diet reduced postprandial glucose area under curve (net AUC) by 60% ( P < 0.001), 24 h glucose by 13% ( P < 0.001), fasting IP and SP concentrations (both absolute and relative to C-peptide, P < 0.05), and postprandial ISR (24%, P = 0.015), while IGI and B up improved by 31% and 45% (both P < 0.001). The CRHP diet increased postprandial glucagon net AUC by 235% ( P < 0.001), subjective satiety by 18% ( P = 0.03), delayed gastric emptying by 15 min ( P < 0.001), decreased gastric inhibitory polypeptide net AUC by 29% ( P < 0.001), but had no significant effect on glucagon-like-peptide-1, total peptide YY, and cholecystokinin responses. A CRHP diet reduced glucose excursions and improved β-cell function, including proinsulin processing, and increased subjective satiety in patients with T2D.

OriginalsprogEngelsk
TidsskriftAmerican Journal of Physiology: Endocrinology and Metabolism
Vol/bind320
Udgave nummer1
Sider (fra-til)E7-E18
ISSN0193-1849
DOI
StatusUdgivet - 1 jan. 2021

Bibliografisk note

Funding Information:
We thank the study patients for devoted effort making this study possible. We thank Core Biochemical Assay Laboratory at Cambridge University Hospitals National Health Service Foundations Trust for the analyses of intact proinsulin and 32,33 split proinsulin. Permission has been obtained by copyright holder to report previously published data (62). The study was funded by a grant from Arla Food for Health, Institute of Clinical Medicine, Health, Aarhus University, Aarhus, Denmark; Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Copenhagen, Denmark, Dept. of Nutrition, Exercise and Sports, University of Copenhagen, Copenhagen, Denmark; and Copenhagen University Hospital Bispebjerg. Foods included in the meal production were partly supplied by Arla Foods, Jan Import A/S, Royal Greenland, and Danish Crown.

Funding Information:
The study was funded by a grant from Arla Food for Health, Institute of Clinical Medicine, Health, Aarhus University, Aarhus, Denmark; Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Copenhagen, Denmark, Dept. of Nutrition, Exercise and Sports, University of Copenhagen, Copenhagen, Denmark; and Copenhagen University Hospital Bispebjerg. Foods included in the meal production were partly supplied by Arla Foods, Jan Import A/S, Royal Greenland, and Danish Crown.

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