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Eric Ravussin

Publications and source records attributed to Eric Ravussin.

42 records · Page 3Linked to original sources
PubMed2002

Increased fat intake, impaired fat oxidation, and failure of fat cell proliferation result in ectopic fat storage, insulin resistance, and type 2 diabetes mellitus.

It is widely accepted that increasing adiposity is associated with insulin resistance and increased risk of type 2 diabetes. The predominant paradigm used to explain this link is the portal/visceral hypothesis. This hypothesis proposes that increased adiposity, particularly in the visceral depots, leads to increased free fatty acid flux and inhibition of insulin action via Randle's effect in insulin-sensitive tissues. Recent data do not entirely support this hypothesis. As such, two new paradigms have emerged that may explain the established links between adiposity and disease. (A) Three lines of evidence support the ectopic fat storage syndrome. First, failure to develop adequate adipose tissue mass in either mice or humans, also known as lipodystrophy, results in severe insulin resistance and diabetes. This is thought to be the result of ectopic storage of lipid into liver, skeletal muscle, and the pancreatic insulin-secreting beta cell. Second, most obese patients also shunt lipid into the skeletal muscle, the liver, and probably the beta cell. The importance of this finding is exemplified by several studies demonstrating that the degree of lipid infiltration into skeletal muscle and liver correlates highly with insulin resistance. Third, increased fat cell size is highly associated with insulin resistance and the development of diabetes. Increased fat cell size may represent the failure of the adipose tissue mass to expand and thus to accommodate an increased energy influx. Taken together, these three observations support the acquired lipodystrophy hypothesis as a link between adiposity and insulin resistance. (B) The endocrine paradigm developed in parallel with the ectopic fat storage syndrome hypothesis. Adipose tissue secretes a variety of endocrine hormones, such as leptin, interleukin-6, angiotensin II, adiponectin (also called ACRP30 and adipoQ), and resistin. From this viewpoint, adipose tissue plays a critical role as an endocrine gland, secreting numerous factors with potent effects on the metabolism of distant tissues. These two new paradigms provide a framework to advance our understanding of the pathophysiology of the insulin-resistance syndrome.

Adipocytes↗
PubMed2002

Assessing risk factors for obesity between childhood and adolescence: I. Birth weight, childhood adiposity, parental obesity, insulin, and leptin.

OBJECTIVE: To assess the effects of body weight, body composition, parental obesity, and metabolic variables on the development of obesity in a large cohort of 5-year-old Native American children with a high propensity for obesity. METHODS: During the summer months of 1992 to 1995 and again 5 years later, 138 (65 boys and 73 girls) 5-year-old Pima Indian children were studied. Height; weight; body composition; parental obesity; and fasting plasma insulin, glucose, and leptin concentrations were determined at baseline and follow-up. Linear regression models were used to assess the effect of the baseline variables on the development of obesity. RESULTS: At both 5 and 10 years of age, Pima Indian children were heavier and fatter than an age- and gender-matched reference population. All anthropometric and metabolic variables tracked strongly from 5 to 10 years of age (r > or = 0.70). The most significant determinant of percentage of body fat at 10 years of age was percentage of body fat at 5 years of age (R(2) = 0.53). The combined effect of high maternal body mass index, elevated fasting plasma leptin concentrations, and low fasting plasma insulin concentrations at baseline explained an additional 4% of the total variance in adiposity at follow-up. CONCLUSIONS: Although parental obesity and metabolic variables such as insulinemia and leptinemia at baseline account for a small percentage of the variance in adiposity at follow-up, early childhood obesity is the dominant predictor of obesity 5 years later. These results suggest that strategies to prevent childhood obesity must be initiated at a very early age.

Adipose Tissue↗
PubMed2002

Assessing risk factors for obesity between childhood and adolescence: II. Energy metabolism and physical activity.

OBJECTIVE: To assess the effect of energy expenditure, including resting metabolic rate (RMR), total energy expenditure (TEE), and activity energy expenditure (AEE), as well as substrate oxidation (respiratory quotient [RQ]), on the development of obesity in a large cohort of Native American children with a high propensity for obesity. METHODS: During the summer months of 1992 to 1995 and again 5 years later, 138 (65 boys and 73 girls) 5-year-old Pima Indian children were studied. At baseline and follow-up, height and weight were measured; body composition was assessed with the use of 18O dilution; RMR and RQ were assessed with the use of indirect calorimetry; TEE was measured with the use of the doubly-labeled water method; and AEE was calculated (TEE - [RMR + 0.1 x TEE]). In addition, an activity questionnaire was used to assess participation in sporting activities as well as television viewing during the previous year. Linear regression models were used to assess the effects of the baseline variables on the development of obesity. RESULTS: Pima Indian children were markedly overweight at both 5 and 10 years of age. Cross-sectionally, percentage of body fat and body weight at 5 and 10 years of age were negatively correlated with sports participation and positively correlated with television viewing. Most important, there was a marked change in the correlation between body size and activity between 5 and 10 years of age: at age 5 years, weight was positively correlated with AEE and PAL, but at age 10 years, the correlation with AEE was lost and that with PAL was negative. However, prospectively, none of the variables measured at baseline was a predictor of percentage of body fat at age 10 years after adjustment for percentage of body fat at age 5 years. CONCLUSIONS: At age 5 years, obesity is associated with decreased participation in sports and increased television viewing but not with a decreased PAL. At age 10 years, obesity is associated with decreased participation in sports, increased television viewing, and a decreased PAL, suggesting that a decrease in PAL in free-living conditions seems to follow, not precede, the development of obesity.

Adolescent↗
PubMed2002

Neuroimaging and obesity: mapping the brain responses to hunger and satiation in humans using positron emission tomography.

The hypothalamus has a major role in the control of food intake. However, neurotracing studies have shown that the hypothalamus receives input from several other regions of the brain that are likely to modulate its activity. Of particular interest to the understanding of human eating behavior is the possible involvement of the cortex. Using positron emission tomography (PET), we generated functional brain maps of the neuroanatomical correlates of hunger (after a 36-h fast) and satiation (after oral administration of a liquid formula meal) in lean and obese subjects. Results in lean individuals indicate that the neuroanatomical correlates of hunger form a complex network of brain regions including the hypothalamus, thalamus, and several limbic/paralimbic areas such as the insula, hippocampal/parahippocampal formation, and the orbitofrontal cortex. Satiation was associated with preferentially increased neuronal activity in the prefrontal cortex. Our studies also indicate that the brain responses to hunger/satiation in the hypothalamus, limbic/paralimbic areas (commonly associated with the regulation of emotion), and prefrontal cortex (thought to be involved in the inhibition of inappropriate response tendencies) might be different in obese and lean individuals. In conclusion, neuroimaging of the human brain is proving to be an important tool for understanding the complexity of brain involvement in the regulation of eating behavior. PET studies might help to unravel the neuropathophysiology underlying human obesity.

Adolescent↗
PubMedDate not supplied

Body cell mass repletion and improved quality of life in HIV-infected individuals receiving oxandrolone.

BACKGROUND: The aim of this study was to measure changes in body cell mass (BCM) and quality of life in HIV-infected individuals undergoing oxandrolone therapy. Previous studies on oxandrolone have neither quantified changes in BCM using criterion methods nor quality of life using an HIV-specific instrument. METHODS: Twenty-five HIV-infected patients (15 with an AIDS diagnosis) on standard antiretroviral and nutrition management were studied before and an average of 18.6 weeks after the initiation of oxandrolone therapy, as prescribed by their primary care physician for the treatment of weight loss. BCM was estimated from intracellular water measured by multiple dilution. Lean soft tissue mass (LTM) was measured by dual-energy X-ray absorptiometry. Quality of life was evaluated by the Functional Assessment of HIV Infection (FAHI) questionnaire. RESULTS: Significant gains in body weight (2.6 +/- 3.0 kg; p < .0001), BCM (3.6 +/- 3.0 kg; p < .0001), and LTM (3.0 +/- 2.9 kg; p < .0001) occurred over an average course of 18.6 weeks of treatment. Overall quality of life improved (p = .056) and appetite improved (p = .032), both of which were positively associated with weight gain (p = .040 and p = .022, respectively). CONCLUSIONS: This is the first study involving oxandrolone therapy in HIV infection to document changes in quality of life and BCM, the metabolically active component of lean body mass that reflects nutritional status better than other more global body composition parameters. Nutritional status and quality of life can improve in HIV-infected individuals receiving a combined therapeutic approach that includes oxandrolone.

Adult↗