Reduced thermogenesis in obesity

Jung, R. T.; Ps, Shetty; James, W. P. T.; Barrand, Margery A.; Callingham, B. A.

doi:10.1038/279322a0

Cited by 279 publications

(90 citation statements)

References 11 publications

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“…However, the stimulation of heat production largely exceeded the stimulant effect on heart rate and blood pressure. The thermogenic effect of yohimbine in dog (+ 100%) was also large when compared to the effect of other thermogenic drugs used in man (Jung et al, 1979;Acheson et al, 1980;Katzeff & Danforth, 1981). Indeed, the other parameters were also largely increased, particularly NEFA and noradrenaline plasma levels.…”

Section: Discussionmentioning

confidence: 99%

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Thermogenic and lipolytic effect of yohimbine in the dog

Galitzky

Vermorel

Lafontan

et al. 1991

British J Pharmacology

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1 Lipid mobilization during a hypocaloric diet may be enhanced by a pharmacological approach using a2-adrenoceptor antagonists since these drugs are known to increase sympathetic tone and stimulate lipolysis. Studies were undertaken in the dog in order to evaluate the effects of oral yohimbine administration (a2-adrenoceptor antagonist) on heat production, metabolic, endocrinological and cardiovascular parameters.2 Acute oral yohimbine (0.25 or 0.40mg kg ')provoked an increase in plasma non-esterfied fatty acids. The drug increased sympathetic nervous system activity as indicated by the increased level of plasma noradrenaline. These effects persisted during the entire experimental period (4 h). The increase in plasma noradrenaline level was two fold higher with the higher dose of yohimbine (0.4mgkg-1). The plasma adrenaline level was increased only with the higher dose. 3 Yohimbine transiently increased plasma insulin and the effect was dose-dependent. 4 Yohimbine (0.25mg kg-1) enhanced heart rate and arterial blood pressure. 5 The effect of yohimbine on oxygen consumption, carbon dioxide and heat production was determined by indirect calorimetry. The drug (0.25 mg kg-1) increased°2 consumption and CO2 and heat production 30min after its administration and the effect persisted over the experimental period. The respiratory quotient, rather low in the fasting animals, remained unchanged. 6 The present work indicates that thermogenesis and lipid mobilization are enhanced during fasting in the dog by a2-adrenoceptor blockade. Yohimbine also induced a transient increase in plasma insulin level and increased heart rate and blood pressure. The lipid mobilization plus the action on thermogenesis observed after yohimbine draw attention to the putative interest of a2-antagonists in the pharmacological treatment of obesity during restricted calorie intake.

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Section: Discussionmentioning

confidence: 99%

“…The thermogenic capacities of catecholamines and other sympathomimetic drugs have been demonstrated previously. Adrenaline and noradrenaline increase the metabolic rate in man (Jung et al, 1979;Katzeff & Danforth, 1981). Ephedrine (a sympathomimetic drug) also stimulates thermogenesis at a dose of 0.25 mg kg- (Astrup et al, 1985).…”

Section: Discussionmentioning

confidence: 99%

Thermogenic and lipolytic effect of yohimbine in the dog

Galitzky

Vermorel

Lafontan

et al. 1991

British J Pharmacology

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“…There are not many studies of NST Adaptations to low energy intakes PS Shetty S21 responses following energy restriction. In one study NST responses to intravenous NA were found to be unaltered in obese women who lost weight following therapeutic energy restriction (Jung et al, 1979).…”

Section: Adaptive Thermogenesismentioning

confidence: 99%

Adaptation to low energy intakes: the responses and limits to low intakes in infants, children and adults

1999

Eur J Clin Nutr

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Reduction in energy intake below the acceptable level of requirement for an individual results in a series of physiological and behavioural responses, which are considered as an adaptation to the low energy intake. This ability of the human body to adapt to a lowering of the energy intake is without doubt bene®cial to the survival of the individual. However, what is more controversial is the view held by some that the body can metabolically adapt in a bene®cial manner to a lowered intake and consequently that the requirements for energy are variable given the same body size and composition and physical activity levels. Much of this confusion is the result of considerable evidence from studies conducted in well-nourished adults who, for experimental or other reasons, have lowered their intakes and consequently demonstrated an apparently enhanced metabolic ef®ciency resulting from changes in metabolic rates which are disproportionate to the changes in body weight. Similar increases in metabolic ef®ciency are not readily seen in individuals who on long-term marginal intakes, probably from childhood, have developed into short-statured, low-body-weight adults with a different body composition. It would thus appear that the generally used indicator of metabolic ef®ciency in humans, that is a reduced oxygen consumption per unit fat free mass, is fraught with problems since it does not account for variations in contributions from sub-compartments of the fat free mass which include those with high metabolism at rest such as brain and viscera and those with low metabolism at rest such as muscle mass. Metabolic rate per unit fat free mass thus, does not re¯ect true variations in metabolic ef®ciency and is due largely to variations in body composition. This ®nding combined with the evidence that behavioural adaptation in habitual physical activity patterns which occurs on energy restriction is not necessarily bene®cial to the individual raises doubts about the role of adaptation to low intakes in determining one's requirement for energy. The evidence is overwhelming that both in children and adults, changes in body size and composition as well as in levels of habitual physical activity may be the most important consequences of a lowered energy intake and cannot be assumed to be a part of a bene®cial adaptation that in¯uences energy requirements.

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“…A reduction in diet-induced thermogenesis in the obese might be explained by their reduced thermogenic response during SNS stimulation. 13, 14 Blaak et al 10 showed that obese men have an impaired response of lipolysis and lipid oxidation during isoprenaline (non-selective b-agonist) infusion. If the availability of FFA in blood is a limiting factor for thermogenesis, the reduced lipolytic response in obese subjects could explain their reduced increases in lipid oxidation and thermogenesis.…”

Section: Introductionmentioning

confidence: 99%

The effect of an increased free fatty acid concentration on thermogenesis and substrate oxidation in obese and lean men

2001

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OBJECTIVE:To examine whether a certain increase in plasma free fatty acid (FFA) concentration leads to similar increases in lipid oxidation and energy expenditure in obese and lean men. DESIGN: The study protocol consisted of a 30 min baseline period after which subjects received an i.v. bolus of 1000 IE heparin. Then consecutive infusions of 4.9, 9.8 and 19.6 mlakg fat-free mass (FFM) Á min of a lipid heparin mixture were started, each infusion for 30 min. SUBJECTS: Eleven obese and 13 lean men with a mean body mass index (BMI) of 34.2 AE 1.0 ( AE s.e.m.) and 23.9 AE 0.5 kgam 2 and age 46.0 AE 1.0 and 42.6 AE 1.5 y, respectively. MEASUREMENTS: Energy expenditure, respiratory exchange ratio (RER) and carbohydrate and lipid oxidation were continuously measured by indirect calorimetry. At the end of each infusion period, a blood sample was taken for FFA, glycerol, insulin, b-hydroxybutyrate, noradrenaline and adrenaline determination. RESULTS: At baseline, plasma FFA levels were comparable in both groups. Lipid heparin infusion increased plasma FFA concentration by 301 AE 47 mmolal and 332 AE 27 mmolal in obese and lean men. Energy expenditure increased similarly in obese and lean men (0.34 AE 0.08 vs 0.40 AE 0.08 kJamin, NS) during lipid heparin infusion, whereas RER decreased similarly in both groups. Lipid oxidation rates were comparable at baseline and increased similarly in obese and lean men (19 AE 5 vs 13 AE 4 mgamin, NS). Baseline plasma insulin levels were higher in the obese, but did not change during lipid heparin infusion. Plasma b-hydroxybutyrate concentrations were similar at baseline, but increased signi®cantly less in the obese during lipid heparin infusion. Baseline noradrenaline and adrenaline concentrations did not differ signi®cantly between groups. During lipid heparin infusion, plasma noradrenaline levels decreased signi®cantly, but plasma adrenaline levels remained unchanged in both groups. CONCLUSION: A certain increase in plasma FFA concentration leads to similar increases in lipid oxidation and energy expenditure in obese and lean men. The accumulation of fat in obese subjects may therefore be more likely to be due to a defect in adipose tissue lipolysis than a defect in lipid oxidation.

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Reduced thermogenesis in obesity

Cited by 279 publications

References 11 publications

Thermogenic and lipolytic effect of yohimbine in the dog

Thermogenic and lipolytic effect of yohimbine in the dog

Adaptation to low energy intakes: the responses and limits to low intakes in infants, children and adults

The effect of an increased free fatty acid concentration on thermogenesis and substrate oxidation in obese and lean men

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