Diet-induced type II diabetes in C57BL/6J mice

Surwit, Richard S.; Kuhn, Cynthia M.; Cochrane, Christina; McCubbin, James A.; Feinglos, Mark N.

doi:10.2337/diabetes.37.9.1163

Cited by 456 publications

(519 citation statements)

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“…Insulin (483±33 pmol/l) and glucose (12.7±.043 mmol/l) levels were also significantly elevated in the high-fat fed compared with low-fat fed control animals (63.9±12 pmol/l and 7.88±0.63 mmol/l, respectively). These results were similar to those reported previously [14,[16][17][18] and show that the high-fat fed mice used in the growth hormone treatment phase were obese and diabetic before treatment began.…”

Section: Resultssupporting

confidence: 91%

“…Generation of a mouse model of diet-induced obesity and type 2 diabetes Induction of a mouse model of obesity and type 2 diabetes using a high-fat diet has been reported previously [14][15][16][17][18]. We purchased 49 male C57Bl/6 J mice (Jackson Laboratories, Bar Harbor, ME, USA) at 21 days of age and divided them into two experimental groups.…”

Section: Methodsmentioning

confidence: 99%

“…In the current study, an established mouse model of dietinduced obesity and type 2 diabetes [14][15][16][17][18] was used to evaluate the impact of growth hormone treatment on type 2 diabetes. Type 2 diabetic mice (defined here as mice with significantly elevated blood glucose and insulin compared with control mice) were treated with a wide range of growth hormone doses for 6 weeks while maintained on a high-fat diet.…”

Section: Introductionmentioning

confidence: 99%

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Growth hormone improves body composition, fasting blood glucose, glucose tolerance and liver triacylglycerol in a mouse model of diet-induced obesity and type 2 diabetes

et al. 2009

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Aims/hypothesis Growth hormone has been used experimentally in two studies to treat individuals with type 2 diabetes, with both reporting beneficial effects on glucose metabolism. However, concerns over potential diabetogenic actions of growth hormone complicate its anticipated use to treat type 2 diabetes. Thus, an animal model of type 2 diabetes could help evaluate the effects of growth hormone for treating this condition. Methods Male C57BL/6J mice were placed on a high-fat diet to induce obesity and type 2 diabetes. Starting at 16 weeks of age, mice were treated once daily for 6 weeks with one of four different doses of growth hormone. Body weight, body composition, fasting blood glucose, insulin, glucose tolerance, liver triacylglycerol, tissue weights and blood chemistries were determined. Results Body composition measurements revealed a dosedependent decrease in fat and an increase in lean mass. Analysis of fat loss by depot revealed that subcutaneous and mesenteric fat was the most sensitive to growth hormone treatment. In addition, growth hormone treatment resulted in improvement in glucose metabolism, with the highest dose normalising glucose, glucose tolerance and liver triacylglycerol. In contrast, insulin levels were not altered by the treatment, nor did organ weights change. However, fasting plasma leptin and resistin were significantly decreased after growth hormone treatment. Conclusions/interpretation Growth hormone therapy improves glucose metabolism in this mouse model of obesity and type 2 diabetes, providing a means to explore the molecular mechanism(s) of this treatment.

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Section: Resultssupporting

confidence: 91%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Growth hormone improves body composition, fasting blood glucose, glucose tolerance and liver triacylglycerol in a mouse model of diet-induced obesity and type 2 diabetes

et al. 2009

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“…As a preliminary study, we studied glucose tolerance in several inbred strains of mice, such as BALB/c, DBA/2, C3H/He, and C57BL/6 mice at 24 weeks of age. All these strains showed similar glucose tolerance except for C57BL/6 mice which were the most glucose intolerant (data not shown) as previously reported by others [8,11]. Since the C3H/He strain is the second most common strain used as experimental mice after the C57BL/6 strain [12], we chose C3H/ He mice as the control strain.…”

Section: Methodssupporting

confidence: 60%

The NSY mouse: a new animal model of spontaneous NIDDM with moderate obesity

et al. 1995

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SummaryThe NSY (Nagoya-Shibata-Yasuda) mouse was established as an inbred strain of mouse with spontaneous development of diabetes mellitus, by selective breeding for glucose intolerance from outbred Jcl:ICR mice. NSY mice spontaneously develop diabetes mellitus in an age-dependent manner. The cumulative incidence of diabetes is 98 % in males and 31% in females at 48 weeks of age. Neither severe obesity nor extreme hyperinsulinaemia is observed at any age in these mice. Glucose-stimulated insulin secretion was markedly impaired in NSY mice after 24 weeks of age. In contrast, fasting plasma insulin level was higher in male NSY mice than that in male C3H/He mice (545 +73 vs 350+ 40 pmol/1, p < 0.05, at 36 weeks of age). Pancreatic insulin content was higher in male NSY mice than that in male C3H/He mice (76 + 8 vs 52 _+ 5 ng/mg wet weight, p < 0.05, at 36 weeks of age). Morphologically, no abnormal findings, such as hypertrophy or inflammatory changes in the pancreatic islets, were observed in NSY mice at any age. These data suggest that functional changes of insulin secretion in response to glucose from pancreatic beta cells may contribute to the development of non-insulin-dependent diabetes mellitus (NIDDM) in the NSY mouse. Although insulin sensitivity was not measured, fasting hyperinsulinaemia in NSY mice suggests that insulin resistance may also contribute to the pathogenesis of NIDDM. Since these findings are similar to the pathophysiologic features of human NIDDM patients, the NSY mouse is considered to be useful for investigating the pathogenesis and genetic predisposition to NIDDM. [Diabetologia (1995) 38: 503-508] Key words NSY mouse, non-insulin-dependent diabetes mellitus, animal model, insulin secretion, isolated islets.Non-insulin-dependent diabetes mellitus (NIDDM) is a heterogeneous disorder, caused by an interaction of genetic and environmental factors [1][2][3]. This heterogeneity in human NIDDM makes it difficult to clarify the genetics or pathogenesis of the disease. Animal models are invaluable for the analysis of heterogeneous disorders such as diabetes. This is eviReceived: 22 June 1994 and in revised form: 11 October 1994 Corresponding author: Dr. H. Ikegami, Department of Geriatric Medicine, Osaka University Medical School, 2-2 Yamadaoka, Suita, Osaka 565, Japan Abbreviations: NIDDM, Non-insulin-dependent diabetes mellitus; IDDM, insulin-dependent diabetes mellitus; NSY mouse, Nagoya-Shibata-Yasuda mouse.denced by the recent progress in the understanding of the genetics and pathogenesis of insulin-dependent diabetes mellitus by use of excellent animal models, such as the nonobese diabetic (NOD) mouse and the Bio-Breeding (BB) rat [4]. Several animal models for NIDDM have been described. Although recent studies have revealed impaired insulin secretion in GK rats [5][6][7], most of the animal models for NIDDM are characterized by obesity, hyperinsulinaemia and islet hypertrophy [8].The NSY (Nagoya-Shibata-Yasuda) mouse is a spontaneous model of NIDDM with moderate obesity that was establ...

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“…However, animal models are a valuable research tool for examining the relation between beta-cell mass, function and morphology on the one hand and insulin It is well documented that insulin concentrations show large amplitude oscillations in the peripheral circulation with a periodicity of 5 to 15 min [1,2,3], and it has been shown that these oscillations are of importance for insulin action in liver [4], muscle [5,6] and adipose tissues [7]. Since Type II (non-insulin-depenresistance on the other, because carefully controlled studies can involve surgical [10,11,12] or toxicological [10,13,14,15,16,17] induction of diabetes and long-term maintenance on experimental diets can induce insulin resistance and lipotoxicity [18,19,20,21]. An animal model should ideally allow peripheral sampling to assess pulsatility, so that invasive surgery to access portal sampling can be avoided.…”

mentioning

confidence: 99%

The conscious Göttingen minipig as a model for studying rapid pulsatile insulin secretion in vivo

Elander

Sturis

et al. 2002

Diabetologia

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Aims/hypothesis. Pulsatile secretion is important for insulin action and suitable animal models are important tools for examining the role of impaired pulsatile insulin secretion as a possible link between beta-cell mass, function and morphology and insulin resistance. This study examines the vascular sampling site, insulin kinetics, pulsatility and the response to glucose pulse entrainment to evaluate the Göttingen minipig as a model for studying pulsatile insulin secretion. Methods. Basal and glucose entrained insulin secretion was examined in normal minipigs and evaluated by autocorrelation, cross correlation and deconvolution. Results. Cross correlation showed a relation between oscillations in insulin concentrations in the portal and jugular vein in anaesthetised animals (p<0.001 in all animals), confirming the usefulness of jugular vein sampling for pulse detection. Jugular vein sampling in conscious animals showed obvious oscillations allowing estimates of burst shape and insulin kinetics. Glucose entrainment improved the pulsatile pattern (autocorrelation: 0.555±0.148 entrained vs 0. 350±0.197 basal, p=0.054). Deconvolution analysis resolved almost all insulin release as secretory bursts (69±20 basal vs 99.5±1.2% entrained, p<0.01) with a pulse interval (min) of 6.6±2.2 (basal) and 9.4±1.5 (entrained) (p<0.05) and a pulse mass (pmol/l per pulse) which was higher after entrainment (228±117 vs 41.2±18.6 basal, p<0.001). Conclusion/interpretation. The ability to fit kinetic parameters directly by deconvolution of peripheral endogenous insulin concentration time series in combination with the suitability of jugular vein sampling, rapid kinetics and entrainability makes the Göttingen minipig ideal for mechanistic studies of insulin pulsatility and its effects on insulin action. [Diabetologia (2002[Diabetologia ( ) 45:1389[Diabetologia ( -1396 Keywords Pulsatile insulin secretion, insulin kinetics, deconvolution, in vivo model, insulin action. dent) diabetes mellitus is characterized by defects in both insulin secretion and action, impaired pulsatile secretion could be an important link between beta-cell malfunction and impaired insulin action [8]. When addressing the cause of these impairments in humans, studies are often influenced by long-term impaired metabolism, and therefore demonstrate that defects could be secondary. This problem can, to some extent, be circumvented by studying first degree relatives of diabetic patients who are at risk of the disease but are still not affected by the effects of hyperglycaemia [9]. However, animal models are a valuable research tool for examining the relation between beta-cell mass, function and morphology on the one hand and insulin It is well documented that insulin concentrations show large amplitude oscillations in the peripheral circulation with a periodicity of 5 to 15 min [1,2,3], and it has been shown that these oscillations are of importance for insulin action in liver [4], muscle [5,6] and adipose tissues [7]. Since Type II (non-insulin-depen-

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Diet-induced type II diabetes in C57BL/6J mice

Cited by 456 publications

References 0 publications

Growth hormone improves body composition, fasting blood glucose, glucose tolerance and liver triacylglycerol in a mouse model of diet-induced obesity and type 2 diabetes

Growth hormone improves body composition, fasting blood glucose, glucose tolerance and liver triacylglycerol in a mouse model of diet-induced obesity and type 2 diabetes

The NSY mouse: a new animal model of spontaneous NIDDM with moderate obesity

The conscious Göttingen minipig as a model for studying rapid pulsatile insulin secretion in vivo

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