Diet-induced insulin resistance precedes other aspects of the metabolic syndrome

Barnard, R. James; Roberts, Christian K.; Varon, S. M.; Berger, Joshua J.

doi:10.1152/jappl.1998.84.4.1311

Cited by 171 publications

(155 citation statements)

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“…Therefore, an inability to suppress a gluconeogenic enzyme by insulin can initiate many of the disorders associated with syndrome X supporting the hypothesis that insulin resistance can trigger syndrome X. Consumption of a high-fat cafeteria diet caused a more dramatic manifestation of syndrome X probably because high-fat diets induce more severe insulin resistance [14,16]. Our data were indicative of this, showing fasting insulin values three times higher than normal values and hyperglycaemia after eating cafeteria food.…”

Section: Discussionsupporting

confidence: 78%

“…Our data were indicative of this, showing fasting insulin values three times higher than normal values and hyperglycaemia after eating cafeteria food. Others have shown that a high-fat, refined sugar diet can induce insulin resistance and hyperinsulinaemia in Fischer rats after only 2 weeks, followed by hypertriglyceridaemia at 2 months, obesity at 5 months, and hypertension at 12 months [14] illustrating, as we have, that insulin resistance independent of obesity can be the underlying cause of syndrome X. This is also supported by studies in non-obese, insulin-resistant mice lacking insulin receptor substrate-1 (IRS-1) which develop hypertriglyceridaemia and hypertension [26].…”

Section: Discussionmentioning

confidence: 99%

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Features of syndrome X develop in transgenic rats expressing a non-insulin responsive phosphoenolpyruvate carboxykinase gene

et al. 1999

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The term`syndrome X' describes a cluster of abnormalities which include glucose intolerance, obesity (particularly abdominal obesity), hypertension, insulin resistance, and dyslipidaemia characterised by raised and potentially atherogenic concentrations of low-density lipoprotein particles, diminished highdensity lipoprotein concentrations and a raised plasma triglyceride concentration [1,2]. Clinically, syndrome X is also associated with increased plasma uric acid and plasminogen activator inhibitor-1 concentrations, and more recently it has been associated with defects in the innate immune system [3] Abstract Aims/hypothesis. Obesity, glucose intolerance, dyslipidaemia and hypertension are a cluster of disorders (syndrome X) affecting many people. It has been hypothesised that these abnormalities are caused by insulin resistance, but definitive proof is lacking. We have developed transgenic rats in which the rate-limiting gluconeogenic enzyme, phosphoenolpyruvate carboxykinase, is non-insulin responsive. The aim of our study was to investigate whether syndrome X develops in these animals and if a high-fat diet interacts with this genetic defect. Methods. Chow-fed transgenic and control rats aged 1, 3, 6 and 17 months and a subgroup of transgenic and control rats fed chow plus cafeteria foods for 6 months were examined for features of syndrome X. Results. At 3 months, transgenic rats had fasting and postprandial hyperinsulinaemia, mild obesity (in abdominal and, to a lesser extent, peripheral regions) and fasting hypercholesterolaemia. Hypertriglyceridaemia was evident after 6 months while hyperglycaemia was apparent at 17 months. Hypertension had not developed by 17 months. The effect of a high-fat diet on insulin, glucose, body weight and body fat was more dramatic than the effect of the transgene alone while the effect of a high-fat diet on cholesterol and triglyceride was similar to the transgene. This illustrates that a high-fat diet is a potent catalyst for many abnormalities associated with syndrome X. There was no evidence of an additive effect of the high-fat diet plus transgene. Conclusion/interpretation. Therefore rats geneticallyengineered with a non-insulin responsive gluconeogenic enzyme develop several aspects of syndrome X, supporting the hypothesis that insulin resistance initiates this cluster of disorders. [Diabetologia (1999) 42: 419±426]

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Section: Discussionsupporting

confidence: 78%

Section: Discussionmentioning

confidence: 99%

Features of syndrome X develop in transgenic rats expressing a non-insulin responsive phosphoenolpyruvate carboxykinase gene

et al. 1999

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“…We chose this experimental rat model based on our previous results, and literature data (Barnard et al 1998, Obradovic et al 2015b). All metabolic parameters for these rats in response to the treatments administered in this study are detailed in our previous study (Obradovic et al 2015a).…”

Section: Animals and Experimental Treatmentmentioning

confidence: 99%

“…In our study, we used male rats fed a HF diet as a model of obesity-associated IR. In this model the HF diet induces whole body IR/hyperinsulinemia, endothelial dysfunction and hypertension (Barnard et al 1998, Panchal et al 2011. Furthermore, we have previously demonstrated using the same male model rats, that a HF diet applied for 10 weeks induces obesity accompanied with abnormalities such as cardiac hypertrophy, increased serum insulin concentration, whole body IR, hyperlipidaemia, hyperleptinemia and inflammation (Obradovic et al 2015a, Obradovic et al 2015b).…”

Section: Introductionmentioning

confidence: 99%

17β-Estradiol protects against the effects of a high fat diet on cardiac glucose, lipid and nitric oxide metabolism in rats

Zafirović

Obradović

Sudar-Milovanović

et al. 2017

Molecular and Cellular Endocrinology

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Please cite this article as: Zafirovic, S., Obradovic, M., Sudar-Milovanovic, E., Jovanovic, A., Stanimirovic, J., Stewart, A.J., Pitt, S.J., Isenovic, E.R., 17β-Estradiol protects against the effects of a high fat diet on cardiac glucose, lipid and nitric oxide metabolism in rats, Molecular and Cellular Endocrinology (2017), doi: 10.1016/j.mce.2017 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. AbstractThe aim of this study was to investigate the in vivo effects of estradiol (E 2 ) on myocardial metabolism and inducible nitric oxide synthase (iNOS) expression/activity in obese rats. MaleWistar rats were fed with a normal or a high fat (HF) diet (42% fat) for 10 weeks. Half of the HF fed rats were treated with a single dose of E 2 while the other half were placebo-treated. 24h after treatment animals were sacrificed. E 2 reduced cardiac free fatty acid (FFA Akt, protein kinase B; AS160, Akt substrate of 160 kDa; CD36, fatty acid transporters; E 2 ,

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“…In Tehran, Iran, it has been estimated to occur in Ͼ30% of adults (5), a prevalence significantly higher than that of most developed countries (6). In choosing a therapeutic diet for metabolic syndrome, all the abnormalities of the metabolic syndrome should be taken into account (7,8). Most patients with the metabolic syndrome are overweight or obese, especially upper-body obese (9,10).…”

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confidence: 99%

Beneficial Effects of a Dietary Approaches to Stop Hypertension Eating Plan on Features of the Metabolic Syndrome

Mirmiran²,

et al. 2005

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OBJECTIVE -To determine the effects of a Dietary Approaches to Stop Hypertension (DASH) eating plan on metabolic risks in patients with the metabolic syndrome.RESEARCH DESIGN AND METHODS -This was a randomized controlled outpatient trial conducted on 116 patients with the metabolic syndrome. Three diets were prescribed for 6 months: a control diet, a weight-reducing diet emphasizing healthy food choices, and the DASH diet with reduced calories and increased consumption of fruit, vegetables, low-fat dairy, and whole grains and lower in saturated fat, total fat, and cholesterol and restricted to 2,400 mg Na. The main outcome measures were the components of the metabolic syndrome.RESULTS -Relative to the control diet, the DASH diet resulted in higher HDL cholesterol (7 and 10 mg/dl), lower triglycerides (Ϫ18 and Ϫ14 mg/dl), systolic blood pressure (SBP) (Ϫ12 and Ϫ11 mmHg), diastolic blood pressure (Ϫ6 and Ϫ7 mmHg), weight (Ϫ16 and Ϫ14 kg), fasting blood glucose (FBG) (Ϫ15 and Ϫ8 mg/dl), and weight (Ϫ16 and Ϫ15 kg), among men and women, respectively (all P Ͻ 0.001). The net reduction in triglycerides (Ϫ17 and Ϫ18 mg/dl), SBP (Ϫ11 and Ϫ11 mmHg), diastolic blood pressure (Ϫ5 and Ϫ6 mmHg), and FBG (Ϫ4 and Ϫ6 mg/dl), weight (Ϫ16 and Ϫ15 kg), and increase in HDL (5 and 10 mg/dl) among men and women, respectively, was higher in the DASH group (all P Ͻ 0.05). The weight-reducing diet resulted in significant change in triglycerides (Ϫ13 and Ϫ10 mg/dl), SBP (Ϫ6 and Ϫ6 mmHg), and weight (Ϫ13 and Ϫ12 kg) among men and women, respectively (all P Ͻ 0.05).CONCLUSIONS -The DASH diet can likely reduce most of the metabolic risks in both men and women; the related mechanisms need further study. Diabetes Care 28:2823-2831, 2005T he metabolic syndrome is a clustering of metabolic abnormalities and cardiovascular risk factors that occur in individuals with impaired insulin sensitivity (1,2). Existing data suggest that the incidence is rising at an alarming rate (3,4). In Tehran, Iran, it has been estimated to occur in Ͼ30% of adults (5), a prevalence significantly higher than that of most developed countries (6). In choosing a therapeutic diet for metabolic syndrome, all the abnormalities of the metabolic syndrome should be taken into account (7,8). Most patients with the metabolic syndrome are overweight or obese, especially upper-body obese (9,10). Therefore, basic weight reduction should be recommended (11). Weight reduction usually improves insulin sensitivity and all the metabolic and cardiovascular abnormalities linked with insulin resistance as well (12). Improvement of insulin sensitivity due to weight reduction is reported before (13). Although weight reduction is an effective way for the treatment of the metabolic syndrome, intervention studies are still needed to determine a specific therapeutic diet for the metabolic syndrome (7). Esposito et al. (14) reported that a Mediterraneanstyle diet might be effective in reducing the prevalence of the metabolic syndrome. Riccardi and Rivellese (7) introduced a diet with high amounts...

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Diet-induced insulin resistance precedes other aspects of the metabolic syndrome

Cited by 171 publications

References 51 publications

Features of syndrome X develop in transgenic rats expressing a non-insulin responsive phosphoenolpyruvate carboxykinase gene

Features of syndrome X develop in transgenic rats expressing a non-insulin responsive phosphoenolpyruvate carboxykinase gene

17β-Estradiol protects against the effects of a high fat diet on cardiac glucose, lipid and nitric oxide metabolism in rats

Beneficial Effects of a Dietary Approaches to Stop Hypertension Eating Plan on Features of the Metabolic Syndrome

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