ArticleJournal of diabetes investigation2012
Augmented reduction of islet β-cell mass in Goto-Kakizaki rats fed high-fat diet and its suppression by pitavastatin treatment.
Article in Journal of diabetes investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Pathological evaluation of the pathogenesis of diabetes mellitus and diabetic peripheral neuropathy.Pathology international · 2024Review
- Prevalence and Risk Factors of Type 2 Diabetes and Prediabetes Among 53,288 Middle-Aged and Elderly Adults in China: A Cross-Sectional Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Article
- Increases in bioactive lipids accompany early metabolic changes associated with β-cell expansion in response to short-term high-fat diet.American journal of physiology. Endocrinology and metabolism · 2018Article
- MIF May Participate in Pathogenesis of Polycystic Ovary Syndrome in Rats through MAPK Signalling Pathway.Current medical science · 2018Article
- Statins and New-Onset Diabetes Mellitus: LDL Receptor May Provide a Key Link.Frontiers in pharmacology · 2017Article
- Age-associated changes of islet endocrine cells and the effects of body mass index in Japanese.Journal of diabetes investigation · 2014Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledAims/Introduction: High fat diet (HFD) is known to be a risk for development of type 2 diabetes. It is unclear, however, how it affects the glucose tolerance or the islet structure in type 2 diabetes. The aim of this study is: (i) to examine the effects of HFD on the islet in GK rats, non-obese type 2 diabetic model; and (ii) to explore if pitavastatin treatment influences the change. MATERIALS AND
methodsTo see the effects of HFD on islet changes in type 2 diabetes, 4-week old male GK and Wistar rats were fed HFD for 16 weeks and subjected to glucose tolerance tests and pathological studies of the islet. The effects of pitavastatin (3 mg/kg/day for 16 weeks, oral), one of the lipophilc statins, were also examined in both GK and Wistrar rats fed with or without HFD.
resultsThe HFD induced hyperlipidemia and aggravated glucose intolerance in both GK and Wistar rats. Pitavastatin treatment did not influence the glucose tolerance in HFD-fed animals. HFD caused an increase in hepatic lipid contents in all the animals, which was partially suppressed by pitavastatin treatment. GK rats showed reduced β-cell mass, and fibrosis and macrophage migration in the islets. HFD feeding in GK rats augmented these changes which were associated with enhanced expression of 8-hydroxydeoxyguanosine and an increase in apoptotic cells. Pitavastatin treatment improved the HFD-induced islet pathology, and pancreatic insulin contents paralleled the structural changes.
conclusionsHFD feeding worsened the islet pathology in GK rats which was suppressed by pitavastatin treatment. (J Diabetes Invest, doi: 10.1111/j.2040-1124.2011.00173.x, 2011).
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