EFFECT OF DIETARY-PROTEIN INTAKE ON INSULIN-SECRETION AND GLUCOSE-METABOLISM IN INSULIN-DEPENDENT DIABETES-MELLITUS

Citation
T. Linn et al., EFFECT OF DIETARY-PROTEIN INTAKE ON INSULIN-SECRETION AND GLUCOSE-METABOLISM IN INSULIN-DEPENDENT DIABETES-MELLITUS, The Journal of clinical endocrinology and metabolism, 81(11), 1996, pp. 3938-3943
Citations number
42
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
0021972X
Volume
81
Issue
11
Year of publication
1996
Pages
3938 - 3943
Database
ISI
SICI code
0021-972X(1996)81:11<3938:EODIOI>2.0.ZU;2-5
Abstract
Adult-onset insulin dependent diabetes mellitus (IDDM) is associated w ith significant residual insulin secretion. The process leading to the ultimate destruction of B cells may be influenced, among other factor s, by the quality and amount of ingested protein. Using a standardized food questionnaire, we matched 13 individuals with normal protein (NP ; 0.74 +/- 0.08 g/kg day) and high protein (KP; 1.87 +/- 0.26 g/kg day ) intake from a sample of 117 newly diagnosed IDDM patients according to sex, age, body mass index, and energy intake. Nondiabetic control s ubjects were also selected. Dietary habits did not change significantl y over an observation period of 1 yr. Glucagon-stimulated C peptide wa s significantly higher in the hrp compared to the HP group (0.71 +/- 0 .06 vs. 0.50 +/- 0.04 nmol/L; P < 0.002). NP food was associated with higher overall insulin sensitivity in both patients and nondiabetic su bjects. Hepatic glucose output was significantly increased in individu als with HP intake [HP IDDM, 14.8 +/- 0.6 vs. NP IDDM, 12.7 +/- 0.7 (P < 0.01); HP control, 12.2 +/- 0.5 vs. NP control, 10.9 +/- 0.5 (P < 0 .01 mu mol/kg . min). Insulin-mediated suppression of hepatic glucose production was impaired in diabetic patients with high protein intake, but not in patients with normal protein diet. Gluconeogenesis estimat ed from C-13 enrichment in breath and plasma was increased in individu als on a HP diet. We conclude that a NP diet is accompanied by delayed progression of the continuous loss of endogenous insulin in IDDM. Thi s phenomenon is possibly due to decreased insulin demand on the B cell s and/or reduced hepatic glucose production favoring enhanced insulin sensitivity.