High-fat-diet-induced Remission of Diabetes in a Subset of K -GOF Insulin-secretory-deficient Mice

Overview

Journal Diabetes Obes Metab

Specialty Endocrinology

Date 2018 Jun 14

PMID 29896801

Citations 5

Authors

Zihan Yan

Zeenat A Shyr

Manuela Fortunato

Alecia Welscher

Mariana Alisio

Michael Martino

Brian N Finck

Hannah Conway

Maria S Remedi

Affiliations

Soon will be listed here.

Abstract

Aims: To examine the effects of a high-fat-diet (HFD) on monogenic neonatal diabetes, without the confounding effects of compensatory hyperinsulinaemia.

Methods: Mice expressing K channel gain-of-function (K -GOF) mutations, which models human neonatal diabetes, were fed an HFD.

Results: Surprisingly, K -GOF mice exhibited resistance to HFD-induced obesity, accompanied by markedly divergent blood glucose control, with some K -GOF mice showing persistent diabetes (K -GOF-non-remitter [NR] mice) and others showing remission of diabetes (K -GOF-remitter [R] mice). Compared with the severely diabetic and insulin-resistant K -GOF-NR mice, HFD-fed K -GOF-R mice had lower blood glucose, improved insulin sensitivity, and increased circulating plasma insulin and glucagon-like peptide-1 concentrations. Strikingly, while HFD-fed K -GOF-NR mice showed increased food intake and decreased physical activity, reduced whole body fat mass and increased plasma lipids, K -GOF-R mice showed similar features to those of control littermates. Importantly, K -GOF-R mice had restored insulin content and β-cell mass compared with the marked loss observed in both HFD-fed K -GOF-NR and chow-fed K -GOF mice.

Conclusion: Together, our results suggest that restriction of dietary carbohydrates and caloric replacement by fat can induce metabolic changes that are beneficial in reducing glucotoxicity and secondary consequences of diabetes in a mouse model of insulin-secretory deficiency.

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