Obesity and the Insulin Resistance Syndrome

Landsberg, Lewis

doi:10.1291/hypres.19.supplementi_s51

Cited by 25 publications

(28 citation statements)

References 32 publications

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“…This hypothesis comes from the evidence that, in experimental animals as well as in humans, acute systemic administration of insulin, performed without affecting glucose levels in the context of the so-called euglygemic clamp approach, triggers a marked sympathetic stimulation (32)(33)(34)(35). Several data further support the abovementioned hypothesis.…”

Section: Fig 3 Muscle Sympathetic Nerve Traffic (Msna) Plasma Norementioning

confidence: 93%

“…It has also been hypothesized that the sympathetic overactivity occurring in metabolic syndrome is dependent on the hyperinsulinemia and the related insulin resistance state characterizing the disease (32). This hypothesis comes from the evidence that, in experimental animals as well as in humans, acute systemic administration of insulin, performed without affecting glucose levels in the context of the so-called euglygemic clamp approach, triggers a marked sympathetic stimulation (32)(33)(34)(35).…”

Section: Fig 3 Muscle Sympathetic Nerve Traffic (Msna) Plasma Norementioning

confidence: 99%

“…Finally, as discussed below, the effects of antihypertensive drugs on adrenergic drive (sympathoexcitation or sympathoinhibition) are frequently mirrored by their impact on insulin sensitivity (worsening or improvement) ( Table 1). A further intriguing finding is that the sympathetic-insulin crosstalks are bidirectional, and at present it is still unknown whether the sympathetic activation is responsible for the insulin resistance state or whether it represents an epiphenomenon of the metabolic alteration (32,33,37).…”

Section: Fig 3 Muscle Sympathetic Nerve Traffic (Msna) Plasma Norementioning

confidence: 99%

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Sympathetic Overdrive and Cardiovascular Risk in the Metabolic Syndrome

Grassı

2006

Hypertens Res

121

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Section: Fig 3 Muscle Sympathetic Nerve Traffic (Msna) Plasma Norementioning

confidence: 93%

Section: Fig 3 Muscle Sympathetic Nerve Traffic (Msna) Plasma Norementioning

confidence: 99%

Section: Fig 3 Muscle Sympathetic Nerve Traffic (Msna) Plasma Norementioning

confidence: 99%

See 1 more Smart Citation

Sympathetic Overdrive and Cardiovascular Risk in the Metabolic Syndrome

Grassı

2006

Hypertens Res

121

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“…[7][8][9] Abdominal obesity is also highly correlated with impairment of body homeostasis characterized by abnormalities such as hyperinsulinaemia, glucose intolerance and dyslipidaemias (hypertriglyceridaemia, high levels of low-density lipoprotein and low levels of high-density cholesterol). [10][11][12][13][14][15] Abdominal obesity, defined as waist circumference value of 102 cm or greater in men, and 88 cm or greater in women is associated with increased relative risk for obesity comorbidities for most adults. 1 Proposed originally by Lean et al 16 and Han et al, 17 these waist circumference cut points were proposed for health promotion to give optimal enrichment to individuals in need of weight management because of overweight/obesity or central obesity.…”

Section: Introductionmentioning

confidence: 99%

Racial/ethnic differences in prehypertension in American adults: Population and relative attributable risks of abdominal obesity

et al. 2004

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To estimate the risk and population attributable risk of prehypertension that is due to abdominal obesity in White, Black and Hispanic American adults. To determine how much of the relative difference in the risk of prehypertension between high-risk Blacks and Hispanics and the low-risk group Whites that is attributable to their differences in abdominal obesity. Data (n ¼ 4016) from the 1999 to 2000 US National Health and Nutrition Examination Surveys were used in this study. Abdominal obesity was defined as waist circumference X102 and X88 cm in men and women, respectively. Prehypertension was defined as not being on antihypertensive medication and having systolic blood pressure of 120-139 mmHg or diastolic blood pressure of 80-89 mmHg. Odds ratio from the logistic regression analysis was used to estimate the risk of prehypertension that was due to abdominal obesity. To estimate prehypertension risk differences between low-risk Whites and high-risk Blacks and Hispanics that was due to abdominal obesity, we estimated relative attribu- The analogous values for women were B39.7 and B16.5%, respectively. In conclusion, despite having lower rates of abdominal obesity than their counterparts, Black men, Hispanic men and Hispanic women had high population attributable risks, indicating that factors other than abdominal obesity may have important explanatory power for racial differences in prehypertension in these groups. However, in Black women reduction in risk of prehypertension could be possible by instituting public health measures to reduce abdominal obesity to the levels seen in White women. Intervention programmes designed to reduce overall obesity may also lead to reduction of abdominal obesity, and consequently may curb prehypertension in these population groups. Lifestyle modification, including diet and exercise, may have public health significance in reducing the incidence of prehypertension in these populations.

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“…The new products, Rosiglitazone (Avandia) and Pioglitazone (Actos), have no cases of liver toxicity but have increased risk of heart failure. [16][17][18] It is therefore important to reduce the cardiac side effects of TZD when it is applied clinically. Potassium channels are found in most cells and their malfunction can lead to various diseases, including epilepsy, diabetes, and hypertension.…”

Section: Discussionmentioning

confidence: 99%

Effects of Metformin on Rosiglitazone-Induced Cardiac Hypertrophy in Mice

Lee

Yeh

Chen³

et al. 2010

Biological & Pharmaceutical Bulletin

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Thiazolidinediones (TZD) can cause adipose tissue accumulation and myocardial hypertrophy. This study aimed to determine if combined Metformin (Glucophage) and Rosiglitazone (Avandia) could reduce the risk of heart failure caused by Rosiglitazone in BALB/c mice. BALB/c mice were treated with oral Rosiglitazone/Metformin twice daily for four weeks. Metformin or Rosiglitazone alone and non-treated mice acted as double control. Myocardial hypertrophy and associated side effects of the combined therapy were determined through isolated heart and body weights. Reverse transcription-polymerase chain reaction (RT-PCR) and Western blot were applied to evaluate expression of sulfonylurea receptor 2A (SUR2A) and Kir 6.2. The activities of peroxisome proliferator activated receptor a (PPARa) in the myocardium were also observed. Rosiglitazone/Metformin decreased body weight gain and food intake, and inhibited an increasing adipose ratio but did not reduce myocardial hypertrophy. Rosiglitazone increased Kir6.2/SUR2A, Kir6.2/SUR2B, and PPARa gene expression. The Rosiglitazone/Metformin combination further increased these gene expressions, especially PPARa. Metformin inhibits obesity but has no effect in reducing myocardial hypertrophy caused by Rosiglitazone. Whether Metformin can reduce side effects of TZDs in humans warrants further study.

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Obesity and the Insulin Resistance Syndrome

Cited by 25 publications

References 32 publications

Sympathetic Overdrive and Cardiovascular Risk in the Metabolic Syndrome

Sympathetic Overdrive and Cardiovascular Risk in the Metabolic Syndrome

Racial/ethnic differences in prehypertension in American adults: Population and relative attributable risks of abdominal obesity

Effects of Metformin on Rosiglitazone-Induced Cardiac Hypertrophy in Mice

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