Development of muscle insulin resistance after liver insulin resistance in high-fat-fed rats

Kraegen, Edward W.; Clark, Peter W; Jenkins, A. B.; Daley, E. A.; Chisholm, Donald J.; Storlien, L. H.

doi:10.2337/diabetes.40.11.1397

Cited by 258 publications

(283 citation statements)

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“…This relation was lost in multiple regression analysis for the Sandwell group, indicating that metabolic factors other than insulin may be important once hepatic insulin resistance rises [30]. Portal blood NEFA may be one such key factor [31].…”

Section: Discussionmentioning

confidence: 98%

Marked differences in the IGF system that are associated with migration in comparable populations of Gujaratis living in Sandwell, UK, and Gujarat, India

et al. 2005

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Aims/hypotheses: We previously reported independent links between the IGF system and the development of impaired glucose tolerance and cardiovascular risk. This study tests the hypothesis that the lifestyle change which accompanies population migration, with attendant increases in cardiovascular risk, is reflected by changes in the IGF system. Materials and methods: We compared a specific Gujarati community in Sandwell, UK (n=205), with people still resident in the same villages of origin near Navsari, India (n=246). We performed anthropometry and measured fasting plasma insulin, IGF-I, insulin-like growth factor binding protein (IGFBP)-1 and IGFBP-3. Results: Daily calorie intake, BMI and WHR were significantly higher in UK Gujaratis than in Indian Gujaratis. IGFBP-1 was significantly lower in UK migrants (mean 29.5 [95% CI 25.9-33.0] vs 56.5 [50.6-62.5]μg/l; F=48.4, p<0.001). Conversely, fasting insulin, IGFBP-3 and IGF-I were all higher in UK Gujaratis (mean IGF-I 145.9 [138.1-153.6]ng/ml in UK Gujaratis and 100.9 [94.6-107.3] ng/ml in Navsari Gujaratis; F=76.6, p<0.001). These differences were still apparent when adjustment was made for BMI by location for IGF-I (F=57.4, p<0.001) and IGFBP-3 (F=5.7, p=0.02), but were no longer apparent for IGFBP-1 and insulin. At the population level, the decrease in IGFBP-1 for a given increase in insulin was significantly smaller in UK Gujaratis, suggesting greater hepatic insulin resistance in this group. Conclusions/interpretation: Environmental factors have profound effects on circulating IGF system components and on the relationship between IGFBP-1, IGF-I and related metabolic variables. This may have long-term implications for the development of worsening glucose tolerance and cardiovascular disease.

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Section: Discussionmentioning

confidence: 98%

Marked differences in the IGF system that are associated with migration in comparable populations of Gujaratis living in Sandwell, UK, and Gujarat, India

et al. 2005

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“…To investigate this possibility, we fed lean control mice a 60 % high-fat diet. This type of diet has been shown to cause hepatic insulin resistance in rats after only 3 days of feeding [40,41]. The high-fat diet caused an increase in weight gain compared to mice fed a control diet.…”

Section: Discussionmentioning

confidence: 99%

The biochemical basis of increased hepatic glucose production in a mouse model of type 2 (non-insulin-dependent) diabetes mellitus

Andrikopoulos

Proietto

1995

Diabetologia

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SummaryThe mechanism of increased hepatic glucose production in obese non-insulin-dependent diabetic (NIDDM) patients is unknown. The New Zealand Obese (NZO) mouse, a polygenic model of obesity and NIDDM shows increased hepatic glucose production. To determine the mechanism of this phenomenon, we measured gluconeogenesis from U-s4C -glycerol and U-14C-alanine and relevant gluconeogenic enzymes. Gluconeogenesis from glycerol (0.07 + 0.01 vs 0.21 + 0.02 ~tmol 9 min -~ 9 body mass index (BMI) -1, p < 0.005) and alanine (0.57 + 0.07 vs 0.99 _+ 0.07 ~tmol 9 min -1 9 BMI-I,p < 0.005) was elevated in control mice NZO vs as was glycerol turnover (0.25 + 0.02 vs 0.63 + 0.09 ~tmol 9 min -1 9 BM1-1, p < 0.05). Fructose 1,6-bisphosphatase activity (44.2 + 1.9 vs 55.7 + 4.1 nmol. min-S, mg protein -s, p < 0.05) and protein levels (6.9 + 1.1 vs 16.7 + 2.3 arbitrary units, p < 0.01) were increased in NZO mouse livers, as was the activity of pyruvate carboxylase (0.12 + 0.01 vs 0.17 + 0.02 nmol-min -~ 9 mg protein -s, p < 0.05). To ascertain whether elevated lipid supply is responsible for these biochemical changes in NZO mice, we fed lean control mice a 60 % fat diet for 2 weeks. Fat-fed mice were hyperinsulinaemic (76.37 + 4.06 vs 98.00 + 7.07 pmol/1, p = 0.05) and had elevated plasma non-esterified fatty acid levels (0.44 + 0.05 vs 0.59 _+ 0.03 mmol/1, p = 0.05). Fructose 1,6-bisphosphatase activity (43.86+2.54 vs 52.93 + 3.09 nmol-min -1 -mg protein -1, p = 0.05) and protein levels (33.03 _+ 0.96 vs 40,04 + 1.26 arbitrary units, p = 0.005) and pyruvate carboxylase activity (0.10 + 0.003 vs 0.14 + 0.01 nmol. min -1 -mg protein -1, p < 0.05) were elevated in fat-fed mice. We conclude that in NZO mice increased hepatic glucose production is due to elevated lipolysis resulting from obesity. [Diabetologia (1995[Diabetologia ( ) 38: 1389[Diabetologia ( -1396

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“…The chronic consumption of diets rich in saturated fats and in processed sugars (high-fat-andfructose diet, HFFD), particularly high fructose, is strongly associated with a variety of related metabolic diseases including obesity, systemic insulin resistance (InsRes), metabolic syndrome, and type-2 diabetes mellitus. 1,2 These diseases have reached epidemic proportions and increased comorbid conditions such as elevated blood pressure, cardiovascular disease, and inflammation, which in turn lead to a reduced quality and expectancy of life. [3][4][5] Obesity caused by hypercaloric diets may be associated with a diminished ability of cells to respond to the action of insulin, leading to InsRes and metabolic syndrome, characterized by hyperglycemia, dyslipidemia, and compensatory hyperinsulinemia.…”

Section: Introductionmentioning

confidence: 99%

“…[3][4][5] Obesity caused by hypercaloric diets may be associated with a diminished ability of cells to respond to the action of insulin, leading to InsRes and metabolic syndrome, characterized by hyperglycemia, dyslipidemia, and compensatory hyperinsulinemia. 1,6 Several epidemiologic studies have found that patients with obesity and InsRes have an increased risk for diverse cognitive impairments, including cognitive decline, mild cognitive impairment, and even Alzheimer's disease (AD). [7][8][9][10] Studies performed in animal models of diet-induced obesity and InsRes such as longterm HFFD feeding show a deficient execution in memory and learning tasks.…”

Section: Introductionmentioning

confidence: 99%

Short-Term High-Fat-and-Fructose Feeding Produces Insulin Signaling Alterations Accompanied by Neurite and Synaptic Reduction and Astroglial Activation in the Rat Hippocampus

Calvo-Ochoa

Hernández‐Ortega

Ferrera

et al. 2014

J Cereb Blood Flow Metab

128

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Chronic consumption of high-fat-and-fructose diets (HFFD) is associated with the development of insulin resistance (InsRes) and obesity. Systemic insulin resistance resulting from long-term HFFD feeding has detrimental consequences on cognitive performance, neurogenesis, and long-term potentiation establishment, accompanied by neuronal alterations in the hippocampus. However, diet-induced hippocampal InsRes has not been reported. Therefore, we investigated whether short-term HFFD feeding produced hippocampal insulin signaling alterations associated with neuronal changes in the hippocampus. Rats were fed with a control diet or an HFFD consisting of 10% lard supplemented chow and 20% high-fructose syrup in the drinking water. Our results show that 7 days of HFFD feeding induce obesity and InsRes, associated with the following alterations in the hippocampus: (1) a decreased insulin signaling; (2) a decreased hippocampal weight; (3) a reduction in dendritic arborization in CA1 and microtubule-associated protein 2 (MAP-2) levels; (4) a decreased dendritic spine number in CA1 and synaptophysin content, along with an increase in tau phosphorylation; and finally, (5) an increase in reactive astrocyte associated with microglial changes. To our knowledge, this is the first report addressing hippocampal insulin signaling, as well as morphologic, structural, and functional modifications due to short-term HFFD feeding in the rat.

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Development of muscle insulin resistance after liver insulin resistance in high-fat-fed rats

Cited by 258 publications

References 0 publications

Marked differences in the IGF system that are associated with migration in comparable populations of Gujaratis living in Sandwell, UK, and Gujarat, India

Marked differences in the IGF system that are associated with migration in comparable populations of Gujaratis living in Sandwell, UK, and Gujarat, India

The biochemical basis of increased hepatic glucose production in a mouse model of type 2 (non-insulin-dependent) diabetes mellitus

Short-Term High-Fat-and-Fructose Feeding Produces Insulin Signaling Alterations Accompanied by Neurite and Synaptic Reduction and Astroglial Activation in the Rat Hippocampus

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