Glucose storage and oxidation in different degrees of human obesity measured by continuous indirect calorimetry

Felber, J. P.; Meyer, H. U.; Curchod, B; Iselin, Hans; Rousselle, J; Maeder, E.; Pahud, P.; Jéquier, E

doi:10.1007/bf01789111

Cited by 12 publications

(14 citation statements)

References 30 publications

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“…Of the other seven studies that did not find a difference between the two groups of subjects, TEF in obesity was not the primary study goal of three of them (18,27,66). Why the other four studies did not find a difference between the two groups we do not know, but it is probably not due to one specific factor.…”

Section: Multiple Factorsmentioning

confidence: 87%

The Thermic Effect of Food and Obesity: A Critical Review

1997

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DE JONGE, LILIAN, GEORGE BRAY. The thermic effect of food and obesity: A critical review. Obes Res. 199735622-631.This review has examined the factors that influence the thermic effect of food (TEF) by evaluating 49 studies that have compared subjects who are obese with those who are lean. Meal size, meal composition, the nature of the previous diet, insulin resistance, physical activity, and ageing influence TEF. In the studies of individuals who are obese or lean, of those who used intravenous glucose infusions, all but one found an impaired thermic response. A total of 29 out of 49 studies of individuals of normal weight or with obesity were identified where there was no difference in age between the groups, and where the subjects who were "overweight" were clearly obese. Of these 29,22 reported a statistically significant reduction in TEF, 3 studies were not designed to look primarily at the effect of obesity on TEF, and the other 4 may not have had sufficiently palatable meals. From this review, we conclude that the reduction of TEF in obesity is related to the degree of insulin resistance, which may be influenced by a low level of sympathetic activity.

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Section: Multiple Factorsmentioning

confidence: 87%

The Thermic Effect of Food and Obesity: A Critical Review

1997

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“…In accordance with this hypothesis is our finding that FFA concentrations were negatively and inversely associated with blood flow rates independently of obesity (Table IV). Because FFA concentrations are inversely related to glucose oxidation (50)(51)(52) it is possible that the inverse association between blood flow rates and FFA reflects indirectly the association between blood flow and glucose oxidation. Finally, it is possible that insulin has a direct vasodilatory effect thereby increasing blood flow and insulin resistance to this effect is the cause for diminished blood flow rates in human obesity.…”

Section: Discussionmentioning

confidence: 99%

Decreased effect of insulin to stimulate skeletal muscle blood flow in obese man. A novel mechanism for insulin resistance.

Laakso

Edelman²,

Brechtel³

et al. 1990

J. Clin. Invest.

904

646

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Obesity is characterized by decreased rates of skeletal muscle insulin-mediated glucose uptake (IMGU). Since IMGU equals the product of the arteriovenous glucose difference (AVGd) across muscle and blood flow into muscle, reduced blood flow and/or tissue activity (AVGd) can lead to decreased IMGU. To examine this issue, we studied six lean (weight 68±3 kg, mean±SEM) and six obese (94±3 kg) men. The insulin doseresponse curves for whole body and leg IMGU were constructed using the euglycemic clamp and leg balance techniques over a large range of serum insulin concentrations. In lean and obese subjects, whole body IMGU, AVGd, blood flow, and leg IMGU increased in a dose dependent fashion and maximal rates of all parameters were reduced in obese subjects compared to lean subjects. The dose-response curves for whole body IMGU, leg IMGU, and AVGd were right-shifted in obese subjects with an ED50 two-to threefold higher than that of lean subjects for each parameter. Leg blood flow increased approximately twofold from basal 2.7±0.2 to 4.4±0.2 dl/min in lean, P < 0.01, and from 2.5±0.3 to 4.4±0.4 dl/min in obese subjects, P < 0.01. The ED50 for insulin's effect to increase leg blood flow was about fourfold higher for obese (957 pmol/liter) than lean subjects (266 pmol/liter), P < 0.01. Therefore, decreased insulin sensitivity in human obesity is not only due to

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“…Although the quantitative thermogenic effect of physiologically liberated norepinephrine is not known, it is possible that the observed rise in norepinephrine contributed to part of the unexplained rise (35- (6)(7)(8)(9) or diabetic obese subjects (10) (40) and possibly a greater absolute inhibition of gluconeogenesis.…”

Section: Discussionmentioning

confidence: 99%

Thermic effect of infused glucose and insulin in man. Decreased response with increased insulin resistance in obesity and noninsulin-dependent diabetes mellitus.

Ravussin¹,

Bogardus²,

Schwartz³

et al. 1983

J. Clin. Invest.

172

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A B S T R A C T The thermic effect of infused glucose and insulin was measured by combining the hyperinsulinemic euglycemic clamp technique with indirect calorimetry, in 10 normal weight volunteers (group I), 7 obese subjects with normal glucose tolerance (group II), and 13 obese subjects with abnormal glucose tolerance or noninsulin-dependent diabetes mellitus before (group IIIa) and after weight loss of 10.8±0.4 kg (group IIIb).During hyperinsulinemia (760-1,100 pmol/liter), total glucose disposal from combined endogenous production and glucose infusion was 545±49, 441±70, 233±35, 231±31 mg/min and energy expenditure changed by +0.476±0.080, +0.293±0.095, -0.114 ±0.063, and +0.135±0.082 kj/min in group I, II, lIla, and IlIb, respectively. The increased energy expenditure correlated with glucose storage (measured cost of processing the glucose: 1.33 kJ/g). In group IIIa there was no increase in energy expenditure in response to glucose and insulin infusions. After therapy (group IIlb) there was a significant recovery (P < 0.05) of the thermic effect of infused glucose although total glucose disposal was unchanged. It is proposed that the recovered thermic effect of infused insulin/glucose is due to the different contributions of gluconeogenesis in the fasting state and during the glucose clamp before and after weight loss. In addition we hypothesize that some of the lower thermic effect of food reported in obese noninsulin-dependent diabetics may be explained by decreased energy expenditure due to a greater suppression of hepatic gluconeogenesis as well as by lower storage rate.

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Glucose storage and oxidation in different degrees of human obesity measured by continuous indirect calorimetry

Cited by 12 publications

References 30 publications

The Thermic Effect of Food and Obesity: A Critical Review

The Thermic Effect of Food and Obesity: A Critical Review

Decreased effect of insulin to stimulate skeletal muscle blood flow in obese man. A novel mechanism for insulin resistance.

Thermic effect of infused glucose and insulin in man. Decreased response with increased insulin resistance in obesity and noninsulin-dependent diabetes mellitus.

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