Short-Term High-Starch, Low-Protein Diet Induces Reversible Increase in β-cell Mass Independent of Body Weight Gain in Mice.

Atsushi Masuda,Yusuke Seino,Yoshitaka Hayashi,Atsushi Suzuki,Yoshihisa Sugimura,Takeshi Takayanagi,Megumi Shibata,Shihomi Hidaka,Masatoshi Murase

doi:10.3390/nu11051045

Atsushi Masuda, Yusuke Seino + Show 7 more

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https://doi.org/10.3390/nu11051045

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Abstract

Long-term exposure to a high starch, low-protein diet (HSTD) induces body weight gain and hyperinsulinemia concomitantly with an increase in β-cell mass (BCM) and pancreatic islets number in mice; however, the effect of short-term exposure to HSTD on BCM and islet number has not been elucidated. In the present study, we investigated changes in body weight, plasma insulin levels, BCM and islet number in mice fed HSTD for 5 weeks followed by normal chow (NC) for 2 weeks. BCM and islet number were increased in mice fed HSTD for 5 weeks compared with those in mice fed NC. On the other hand, mice fed HSTD for 5 weeks followed by NC for 2 weeks (SN) showed decreased BCM and insulin levels, compared to mice fed HSTD for 7 weeks, and no significant differences in these parameters were observed between SN and the control NC at 7 weeks. No significant difference in body weight was observed among HSTD, NC and SN fed groups. These results suggest that a high-starch diet induces an increase in BCM in a manner independent of body weight gain, and that 2 weeks of NC feeding is sufficient for the reversal of the morphological changes induced in islets by HSTD feeding.

Highlights

Insulin is secreted from pancreatic β-cells, and plays an important role in glucose metabolism.Glucose stimulates insulin secretion directly and indirectly through incretins such as glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) [1]
We previously reported that both wild-type (WT) and GIP receptor-deficient (GiprKO) mice fed a high-starch, low-protein diet (HSTD), show a body weight gain, compared with those fed normal chow (NC), indicating that HSTD induces obesity in a manner independent of the GIP signal [5]
We found that BCM and the number of islets is increased in mice fed HSTD for 22 weeks, which show obesity and hyperglycemia and hyperinsulinemia, and that the expression levels of cyclin D1 and cyclin D2 mRNA in islets are increased in these mice [7]

Summary

Introduction

Glucose stimulates insulin secretion directly and indirectly through incretins such as glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) [1]. Both insulin and GIP contribute to the promotion of fat deposition in adipose tissue [2,3,4]. We previously reported that both wild-type (WT) and GIP receptor-deficient (GiprKO) mice fed a high-starch, low-protein diet (HSTD), show a body weight gain, compared with those fed normal chow (NC), indicating that HSTD induces obesity in a manner independent of the GIP signal [5]. Glucose-induced insulin secretion (GIIS) from isolated islets is enhanced in WT and GiprKO-fed HSTD, compared with those in WT and GiprKO-fed NC or a moderate-fat diet 22 weeks after intervention of the diets [5]

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