Effect of diet change on insulin action: difference between muscles and adipocytes

Maegawa, Hiroshi; Kobayashi, Masashi; Ishibashi, Osamu; Takata, Yasumitsu; Shigeta, Y.

doi:10.1152/ajpendo.1986.251.5.e616

Cited by 28 publications

(22 citation statements)

References 8 publications

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“…We observed hyperglycaemia, hyperinsulinaemia, hyperleptinaemia and insulin resistance during the glucose tolerance test and the euglycaemic-hyperinsulinaemic clamp study. These abnormalities were identical with those reported in the literature (Maegawa et al, 1986;Stevenson et al, 1996;Ghorbani & Himms-Hagen, 1998). In this model, JTT-501 clearly improved the impaired insulin resistance index in the glucose tolerance test, and decreased abnormal serum parameters.…”

Section: Discussionsupporting

confidence: 91%

JTT‐501, a novel oral antidiabetic agent, improves insulin resistance in genetic and non‐genetic insulin‐resistant models

Shibata¹,

Matsui²,

Yonemori³

et al. 1998

British J Pharmacology

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1 We investigated whether ethoxy]benzyl]-3,5-isoxazolidinedione) would improve insulin resistance in genetic (Zucker fatty rats) and non-genetic (high-fat fed rats) rodent models of obesity. 2 JTT-501 (10 ± 100 mg kg 71 day 71 ) was administered orally to Zucker fatty rats for 7 ± 21 days. In the high-fat fed rat model, JTT-501 (100 mg kg 71 day 71 ) was administered orally for 7 days. In both models, JTT-501 improved metabolic abnormalities by enhancing insulin action during the glucose tolerance test and the euglycaemic-hyperinsulinaemic clamp study. In ex vivo assays, JTT-501 ameliorated the impaired insulin-sensitive glucose oxidation and lipid synthesis in peripheral tissues. Furthermore, JTT-501 enhanced insulin receptor autophosphorylation in hindlimb muscle. 3 JTT-501 reduced serum leptin concentrations in both models, but did not aect body weight or epididymal fat weight. 4 Our observations indicate that JTT-501 improves the metabolic abnormalities in both genetic and non-genetic insulin-resistant models by enhancing insulin action in peripheral tissues. These eects of JTT-501 are due, at least in part, to enhanced insulin receptor autophosphorylation. In addition, JTT-501 is able to reduce serum leptin concentrations in hyperleptinaemia of the insulinresistant model. We expect JTT-501 to show promise for treating non-insulin dependent diabetes mellitus patients with insulin resistance.

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Section: Discussionsupporting

confidence: 91%

JTT‐501, a novel oral antidiabetic agent, improves insulin resistance in genetic and non‐genetic insulin‐resistant models

Shibata¹,

Matsui²,

Yonemori³

et al. 1998

British J Pharmacology

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“…Our results suggest that the HD group manifested insulin resistance. Insulin resistance can be generated by alterations in the number of insulin receptors and in insulin signaling (30,31); several researchers have observed that insulin resistance in experimental obesity models may be linked to abnormalities in glucose transporter 4 receptor (GLUT4). This scenario may suggest an abnormality at GLUT4.…”

Section: Discussionmentioning

confidence: 99%

Effects of chronic stress and high-fat diet on metabolic and nutritional parameters in Wistar rats

Bruder‐Nascimento

Campos

Alves

et al. 2013

Arq Bras Endocrinol Metab

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Objective: The aim of this study was assess the role of chronic stress on the metabolic and nutritional profile of rats exposed to a high-fat diet. Materials and methods: Thirty-day-old male Wistar rats (70-100 g) were distributed into four groups: normal-diet (NC), chronic stress (St), high-fat diet (HD), and chronic stress/high-fat diet (HD/St). Stress consisted at immobilization during 15 weeks, 5 times per week, 1h per day; and exposure to the high-fat diet lasted 15 weeks. Nutritional and metabolic parameters were assessed. The level of significance was 5%. Results: The HD group had final body weight, total fat, as well as insulin and leptin increased, and they were insulin resistant. The St and HD/St had arterial hypertension and increased levels of corticosterone. Stress blocked the effects of the high-fat diet. Conclusion: Chronic stress prevented the appearance of obesity. Our results help to clarify the mechanisms involved in metabolic and nutritional dysfunction, and contribute to clinical cases linked to stress and high-fat diet. Arq Bras Endocrinol Metab. 2013;57(8):642-9 Keywords Chronic stress; high-fat diet; calorie intake and food intake RESUMO Objetivo: Avaliar o papel do estresse crônico sobre parâmetros metabólicos e nutricionais de ratos expostos à dieta rica em gordura. Materiais e métodos: Ratos Wistar machos (30 dias de idade/70-100 g) foram distribuídos em quatro grupos: dieta-normal (NC), estresse crônico (St), dieta rica em gordura (HD) e estresse crônico/dieta rica em gordura (HD/St). O estresse consistiu em imobilização durante 15 semanas, 5 vezes por semana 1h por dia e a dieta rica em gordura foi oferecida por 15 semanas. Parâmetros nutricionais e metabólicos foram avaliados. O nível de significância foi de 5%. Resultados: HD tiveram peso corpóreo, gordura total e níveis de insulina e leptina aumentados e foram resistentes à insulina. Os grupos St e HD/St manifestaram hipertensão e níveis séricos de corticosterona elevados. O estresse bloqueou os efeitos da dieta. Conclusão: O estresse impediu o surgimento dela. Nossos resultados ajudam compreender os mecanismos envolvidos na disfunção metabólica e nutricional e contribuem para casos clínicos de estresse e dietas ricas em gorduras. Arq Bras Endocrinol Metab. 2013;57(8):642-9 Descritores Estresse crônico; dieta rica em gordura; consumo calórico e metabolismo

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“…Assessment of in Vivo Insulin Sensitivity-To assess in vivo insulin sensitivity, we performed the insulin sensitivity test using constant glucose, insulin, and somatostatin infusion (22). This test proposes that endogenous insulin secretion is suppressed with somatostatin coupled with a fixed constant glucose and insulin infusion.…”

Section: Materials-purifiedmentioning

confidence: 99%

“…Assessment of Glucose Uptake into Isolated Soleus Muscle-Glucose transport activity was assessed by the measurement of 2-deoxyglucose uptake as described (22). In brief, soleus muscle was separated from hindlimb and incubated with insulin (0 -10 nM) at 25°C in 2 ml of Krebs-Ringer phosphate (KRP) buffer containing 10 mM HEPES and 11 mM glucose for 120 min.…”

Section: Materials-purifiedmentioning

confidence: 99%

Expression of a Dominant Negative SHP-2 in Transgenic Mice Induces Insulin Resistance

Maegawa

Hasegawa

Sugai

et al. 1999

Journal of Biological Chemistry

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To elucidate the roles of SHP-2, we generated transgenic (Tg) mice expressing a dominant negative mutant lacking protein tyrosine phosphatase domain (⌬PTP). On examining two lines of Tg mice identified by Southern blot, the transgene product was expressed in skeletal muscle, liver, and adipose tissues, and insulin-induced association of insulin receptor substrate 1 with endogenous SHP-2 was inhibited, confirming that ⌬PTP has a dominant negative property. The intraperitoneal glucose loading test demonstrated an increase in blood glucose levels in Tg mice. Plasma insulin levels in Tg mice after 4 h fasting were 3 times greater with comparable blood glucose levels. To estimate insulin sensitivity by a constant glucose, insulin, and somatostatin infusion, steady state blood glucose levels were higher, suggesting the presence of insulin resistance. Furthermore, we observed the impairment of insulin-stimulated glucose uptake in muscle and adipocytes in the presence of physiological concentrations of insulin. Moreover, tyrosine phosphorylation of insulin receptor substrate-1 and stimulation of phosphatidylinositol 3-kinase and Akt kinase activities by insulin were attenuated in muscle and liver. These results indicate that the inhibition of endogenous SHP-2 function by the overexpression of a dominant negative mutant may lead to impaired insulin sensitivity of glucose metabolism, and thus SHP-2 may function to modulate insulin signaling in target tissues. SHP-2 (also referred to as PTP1D, PTP2C, SHPTP2, or SYP)is a ubiquitously expressed protein-tyrosine phosphatase (PTPase) 1 containing a single PTPase domain and two adjacent Src homology (SH) 2 domains near its N terminus which specifically associate with a variety of tyrosine-phosphorylated proteins upon growth factor stimulation (1-5). SHP-2 is the mammalian homologue of Drosophila Corkscrew, whose gene product potentiates the Drosophila homologue of mammalian c-raf to positively transmit signals downstream of the Torso receptor tyrosine kinase (6). Furthermore, SHP-2 has been reported to play an important role in mesodermal induction in oocyte by regulation of mitogen-activated protein (MAP) kinase activity (7).Regarding the roles of SHP-2 in tyrosine kinase signaling, several lines of evidence indicate that SHP-2 acts as a positive mediator in growth factor signaling such as that by plateletderived growth factor and epidermal growth factor (4,5,8,9). After stimulation by these ligands, SHP-2 is tyrosine-phosphorylated and bound to Grb2-SOS complex, resulting in activation of p21 ras and MAP kinase cascade. On the other hand, in the case of insulin signaling, SHP-2 is not tyrosine-phosphorylated in response to insulin stimulation. However, insulin induces the association of IRS-1 with SHP-2 (10, 11), and the expression of either a catalytically inactive mutant SHP-2 (Cys/Ser) or a deletion mutant lacking PTPase domain in Chinese hamster ovary cells overexpressing insulin receptors (CHO-IR) results in the attenuation of the insulin-stimulated MAP kinase activity, ...

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Effect of diet change on insulin action: difference between muscles and adipocytes

Cited by 28 publications

References 8 publications

JTT‐501, a novel oral antidiabetic agent, improves insulin resistance in genetic and non‐genetic insulin‐resistant models

JTT‐501, a novel oral antidiabetic agent, improves insulin resistance in genetic and non‐genetic insulin‐resistant models

Effects of chronic stress and high-fat diet on metabolic and nutritional parameters in Wistar rats

Expression of a Dominant Negative SHP-2 in Transgenic Mice Induces Insulin Resistance

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