High-fat diet feeding significantly attenuates anagliptin-induced regeneration of islets of Langerhans in streptozotocin-induced diabetic mice

Takanori Shinjo, Yusuke Nakatsu, Misaki Iwashita, Tomomi Sano, Hideyuki Sakoda, Hisamitsu Ishihara, Akifumi Kushiyama, Midori Fujishiro, Fusanori Nishimura, Tomoichiro Asano

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Background: DPP-4 inhibitors reportedly exert effects on both alpha and beta cells, and promote the proliferation and survival of beta cells. We investigated the effects of anagliptin on structurally-impaired islets of Langerhans in streptozotocin (STZ)-treated mice, fed either a normal or a high-fat diet. Pdx-1 expression in the pancreas and serum insulin/glucagon concentrations were also examined. Findings: Anagliptin treatment significantly up-regulated pancreatic Pdx-1 expression, with elevated serum glucagon-like peptide-1 concentrations, regardless of whether the diet was normal or high-fat. However, interestingly, the beta cell regeneration, structural normalization of islets of Langerhans including alpha cell: beta cell area ratios, and serum insulin elevation, all observed with anagliptin administration in the animals fed a normal diet, were markedly suppressed in the high-fat fed group. Conclusions: High-fat diet feeding clearly weakened the regenerative effects of anagliptin on the islets of Langerhans in STZ-treated mice. Our findings suggest the importance of normalizing lipid metabolism for full manifestation of DPP-4 inhibitor effects on the islets of Langerhans.

Original languageEnglish
Article number50
JournalDiabetology and Metabolic Syndrome
Volume7
Issue number1
DOIs
Publication statusPublished - Jun 2 2015

All Science Journal Classification (ASJC) codes

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

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