Selective breeding of mice for different susceptibilities to high fat diet‐induced glucose intolerance: Development of two novel mouse lines, Selectively bred Diet‐induced Glucose intolerance‐Prone and ‐Resistant

Nagao, Mototsugu; Asai, Akira; Kawahara, Momoyo; Sato, Yuki; Tanimura, Kyoko; Okajima, Fumitaka; Takaya, Makiyo; Sudo, Mariko; Takemitsu, Shuji; Harada, Taro; Sugihara, Hitoshi; Oikawa, Shinichi

doi:10.1111/j.2040-1124.2011.00175.x

Cited by 12 publications

(15 citation statements)

References 24 publications

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“…Thus, there are individual differences to the susceptibility to develop T2D by HFD. To investigate this question Nagao and co-workers have developed mouse lines with distinctively different susceptibilities (prone and resistant) to HFD-induced glucose intolerance [59]. The two mice strains are called ''selectively bred diet-induced glucose intolerance-prone (SDG-P)'' and ''-resistant (SDG-R)''.…”

Section: Impact Of Obesity On First Phase Insulin Secretion and Beta mentioning

confidence: 99%

Lessons from basic pancreatic beta cell research in type-2 diabetes and vascular complications

2017

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The changes in lifestyle with increased access of food and reduced physical activity have resulted in the global epidemic of obesity. Consequently, individuals with type 2 diabetes and cardiovascular disease have also escalated. A central organ in the development of diabetes is the pancreas, and more specifically the pancreatic beta cells within the islets of Langerhans. Beta cells have been assigned the important task of secreting insulin when blood glucose is increased to lower the glucose level. An early sign of diabetes pathogenesis is lack of first phase insulin response and reduced second phase secretion. In this review, which is based on the foreign investigator award lecture given at the JSDC meeting in Sendai in October 2016, we discuss a possible cellular explanation for the reduced first phase insulin response and how this can be influenced by lipids. Moreover, since patients with cardiovascular disease and high levels of cholesterol are often treated with statins, we summarize recent data regarding effects on statins on glucose homeostasis and insulin secretion. Finally, we suggest microRNAs (miRNAs) as central players in the adjustment of beta cell function during the development of diabetes. We specifically discuss miRNAs regarding their involvement in insulin secretion regulation, differential expression in type 2 diabetes, and potential as biomarkers for prediction of diabetes and cardiovascular complications. Keywords Insulin secretion Á Exocytosis Á Beta cell Á Obesity Á Statin Á MicroRNA/miRNA The original version of this article was revised: The text including the subheading ''Statins and insulin sensitivity'' was transposed incorrectly and it has been updated in this article.

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Section: Impact Of Obesity On First Phase Insulin Secretion and Beta mentioning

confidence: 99%

Lessons from basic pancreatic beta cell research in type-2 diabetes and vascular complications

2017

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“…kines in the visceral fat, higher blood pressure (Fig. 3), and lower HDL-cholesterol levels [99] compared to SDG-R mice. In addition, SDG-P mice fed an atherogenic diet showed greater atherosclerotic lesion formation than SDG-R mice [102].…”

Section: Disclosurementioning

confidence: 91%

“…As a result, 2 mouse lines with distinctively different susceptibilities (prone and resistant) to high-fat diet-induced glucose intolerance (Fig. 2), designated "selectively bred diet-induced glucose intolerance-prone (SDG-P)" and "-resistant (SDG-R)", respectively, were established [99].…”

Section: Selective Breedingmentioning

confidence: 99%

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Fat intake and the development of type 2 diabetes [Review]

et al. 2015

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The increase in the number of patients with diabetes has become a worldwide healthcare issue, with numbers predicted to reach approximately 600 million by 2035. In Asia-Pacific region, the prevalence of type 2 diabetes has increased dramatically in recent decades, of which the major causes are believed to be modern lifestyle changes, e.g., Western dietary pattern and reduced physical activity, on their genetic basis of lower insulin secretory capacity. Particularly, in East Asian countries, the amount of fat intake has increased nearly three-fold over this half of century; dietary fat appears to be the major culprit of type 2 diabetes pandemic in East Asia. However, convincing evidence has not yet been provided as to whether high-fat diet causes type 2 diabetes in epidemiological cohort studies. Here, we summarize clinical studies regarding fat intake and type 2 diabetes, and animal studies on high-fat diet-induced diabetes including our recent works on the novel mouse lines (selectively bred diet-induced glucose intolerance-prone [SDG-P] and -resistant [SDG-R]) to address the etiology of high-fat diet-induced diabetes. These epidemiological and experimental findings would provide further insight into the etiology of type 2 diabetes under the modern nutritional environment, namely in the context of increased fat intake.

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“…Recently, we established 2 mouse lines, with distinctively different susceptibilities to diet-induced glucose intolerance, by selective breeding (designated s electively bred d iet-induced g lucose intolerance- p rone [SDG-P] and- r esistant [SDG-R]) [ 9 , 10 ], and demonstrated that SDG-P mice showed accelerated atherosclerotic lesion formation compared to SDG-R mice [ 11 ]. Since SDG-P mice manifested post-glucose challenge hyperglycemia without overt fasting hyperglycemia, the mice may serve as useful animal models for studying IGT-related disorders.…”

Section: Introductionmentioning

confidence: 99%

Repetitive Glucose Spikes Accelerate Atherosclerotic Lesion Formation in C57BL/6 Mice

et al. 2015

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BackgroundA number of epidemiological studies demonstrated that postprandial hyperglycemia is a risk factor for cardiovascular disease in individuals with impaired glucose tolerance. Although several laboratory studies have addressed the plausible causal role of postprandial acute hyperglycemia (glucose spikes) in the development of atherosclerosis, there is little convincing evidence in vivo whether the atherosclerotic lesion formation can be accelerated solely by glucose spikes. Here, we assessed the effect of repetitive glucose spikes on atherosclerotic lesion formation in mice.MethodsFemale C57BL/6 mice were fed an atherogenic diet from 8 to 28 weeks of age. During the atherogenic diet feeding period, the mice orally received a glucose solution (50 mg glucose/mouse; G group) or water (W group) twice daily, 6 days a week. Atherosclerotic lesion formation in the aortic sinus was quantitatively analyzed in serial cross-sections by oil red O staining.ResultsG group mice showed transient increases in blood glucose level (~5 mmol/L above W group), and the levels returned to levels similar to those in W group mice within 60 min. No significant differences in glucose tolerance, insulin sensitivity, and plasma lipid profiles were observed after the 20-week repetitive administration between the 2 groups. G group mice showed an approximately 4-fold greater atherosclerotic lesion size in the aortic sinus than W group mice. Gene expression levels of Cd68 and Icam1 in the thoracic aorta were higher in G group mice than in W group mice.ConclusionsThese results indicate that glucose spikes can accelerate atherosclerotic lesion formation, with little influence on other metabolic disorders. Repetitive glucose administration in wild-type mice may serve as a simple and useful approach to better understanding the causal role of glycemic spikes in the development of atherosclerosis.

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Selective breeding of mice for different susceptibilities to high fat diet‐induced glucose intolerance: Development of two novel mouse lines, Selectively bred Diet‐induced Glucose intolerance‐Prone and ‐Resistant

Cited by 12 publications

References 24 publications

Lessons from basic pancreatic beta cell research in type-2 diabetes and vascular complications

Lessons from basic pancreatic beta cell research in type-2 diabetes and vascular complications

Fat intake and the development of type 2 diabetes [Review]

Repetitive Glucose Spikes Accelerate Atherosclerotic Lesion Formation in C57BL/6 Mice

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