What causes the insulin resistance underlying obesity?

Hardy, Olga T.; Czech, Michael P.; Corvera, Silvia

doi:10.1097/med.0b013e3283514e13

Cited by 420 publications

(325 citation statements)

References 50 publications

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“…Altered FGF23 levels may also contribute to cardiac remodeling (18). The association of insulin resistance with obesity, mainly visceral obesity, is well known (19)(20)(21)(22). Our research revealed similar correlations, as expected.…”

Section: Discussionsupporting

confidence: 77%

Relationship of Left Ventricular Mass with BMI and Insulin Resistance in Normotensive Obese Women

Altinok¹,

Erdenen²,

Karabağ³

et al. 2016

Istanbul Med J

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The relationship between excess body weight and cardiovascular disease has been well known for years (1)(2)(3)(4)(5). Increasing body mass requires increased cardiac debi and vascular volume to supply metabolic demands (3,6,7). This may be partly due to the altered metabolic needs induced by increased body weight (8).Left ventricular hypertrophy (LVH) may cause diastolic and systolic heart failure; it is also an independent risk factor for cardiac arrhythmia, sudden death, myocardial ischemia, and heart failure (9). LVH in obese people is related to the severity of comorbidities, mainly hypertension. Although obesity itself is an independent risk factor for LVH in hypertensive patients, the roles of excess body weight and obesity in LVH in normotensive subjects are inconclusive (5, 10). In this article, we investigated the relationships of obesity and insulin resistance with LVH and diastolic function in nondiabetic, normotensive women who were followed up at our obesity outpatient clinic; the results were compared with those of normal women. MethodsThis study was conducted at our hospital with 81 obese, nondiabetic, normotensive female subjects (study group) and 36 healthy female controls (control group). All participants were informed about the survey and freely signed and dated the consent form. The protocol was approved by the Local Ethics Committee and was conducted in accordance with the Declaration of Helsinki.Patients were excluded if they had a history of ischemic heart disease, congestive heart failure, cardiac valve disease, liver or kidney disease, hypertension, cancer, adrenal disease (such as Conn's disease, pheochromocytoma, or Cushing's syndrome, which can cause secondary hypertension), diabetes mellitus, thyroid disease, glucose intolerance, malnutrition, or malabsorption.The age, weight, height, body mass index (BMI), waist circumference (WC), systolic and diastolic blood pressure, and heart rate of the subjects were recorded. Serum fasting blood glucose (FBG), Relationship of Left Ventricular Mass with BMI and Insulin Resistance in Normotensive Obese WomenObjective: Obesity is correlated with left ventricular mass (LVM) and insulin resistance (IR) and is an independent predictor of LVM in nondiabetic, nonhypertensive, obese people. Our aim was to investigate the relationship of body mass index (BMI) and IR with left venticular mass index (LVMI) in obese and nonobese, normotensive, nondiabetic women.Methods: 81 obese, normotensive, nondiabetic women and 36 healthy women of normal weight were included in the study. We compared the demographic features, biochemical values, insulin and HOMA-IR values, heart rate, blood pressure, and echocardiographic parameters of the obese and nonobese subjects. Results:The mean age was 39.3±11.2 years and the mean BMI was 39.5±5.7 kg/m 2 in the obese group; the mean age was 38.4±9.5 years and the mean BMI was 22.5±1.9 kg/m 2 in the control group. Hyperinsulinemia (19.3±10.4 µU/mL) and IR (HOMA-IR: 4.6±2.9) were correlated with obesity. Insulin levels and IR were...

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Section: Discussionsupporting

confidence: 77%

Relationship of Left Ventricular Mass with BMI and Insulin Resistance in Normotensive Obese Women

Altinok¹,

Erdenen²,

Karabağ³

et al. 2016

Istanbul Med J

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“…An association between increasing pituitary scores and age was also identified. Obesity is associated with increased oxidative stress in humans [19], and increased concentrations of the acute phase protein SAA have been associated with both obesity and IR in horses [20]. Acute phase proteins are increased as part of the response to inflammatory stimuli, and therefore, obesity may also result in low-grade inflammation and oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Pituitary Lesions, Obesity, and Mesenteric Lipomas in Insulin-Resistant Horses

Newkirk¹,

Chameroy²,

Tadros³

et al. 2014

OJVM

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The aim of the current study was to identify associations between pituitary lesions, body condition scores, and mesenteric lipomas in horses with insulin resistance. Necropsy examinations were performed following euthanasia in 30 adult horses designated as insulin resistant (n = 11) or insulin sensitive (n = 19). Insulin sensitivity was determined using the insulin-modified frequently sampled intravenous glucose tolerance test and resting insulin concentrations. At necropsy, mesenteric lipomas were measured. The pituitary and adrenal glands, pancreas, and liver were evaluated histologically; pituitary glands were scored based on published criteria. Insulin-resistant horses had significantly higher pituitary scores (p = 0.0035) and body condition scores (p = 0.0001), even when adjusting for age, and a greater frequency of mesenteric lipomas (p = 0.014) and greater lipoma area (p = 0.0332) than insulin-sensitive horses. Regardless of insulin status, horses with pituitary scores ≥3 (diffuse hyperplasia; n = 25) had higher body condition scores (p = 0.0313) and a greater frequency of mesenteric lipomas (p < 0.0002) than those with lower pituitary scores. High body condition score was not correlated to an increased frequency of mesenteric lipomas. Detection of higher pituitary scores in insulin-resistant horses suggested an association between insulin resistance and pituitary morphology. Horses in the insulin-resistant group and those with high pituitary scores had higher body condition scores and a greater frequency of mesenteric lipomas. These horses might be at increased risk for lipoma-associated colic.

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“…The discovery of impaired liver IRK activity in obese insulin-resistant humans almost 30 years ago (28,29) suggested IRK regulation as a pathophysiological mechanism for hepatic insulin resistance, but most studies since have focused on post-receptor defects as being central to insulin resistance (30)(31)(32)(33). Distal effectors such as PI3K and AKT have multiple overlapping inputs, so primary defects in PI3K or AKT would blunt many anabolic programs independently of insulin action (34).…”

Section: Discussionmentioning

confidence: 99%