Reduced thermic effect of feeding in obesity: Role of norepinephrine

Schwartz, Robert S.; Halter, Jeffrey B.; Bierman, Edwin L.

doi:10.1016/0026-0495(83)90214-7

Cited by 63 publications

(26 citation statements)

References 13 publications

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“…However, the plasma noradrenaline response promoted by feeding was previously found to be of similar magnitude in obese and control subjects. 20 It can be noticed that the obese patients included in this study had an increased thermogenesis after glucose load (about 8% over the baseline) during placebo administration, close to that previously reported in obese patients. 14 Studies from our group demonstrated that activation of sympathetic tone through administration of the a 2 -adrenoceptor antagonist yohimbine was similar in obese and control subjects.…”

Section: Discussionsupporting

confidence: 85%

“…There is abundant evidence that SNS activation contributes to the thermic effect of glucose 7 in humans: carbohydrate administration increases plasma noradrenaline concentrations 6,19,20 and noradrenaline release in muscle nerves. 21 It has been reported that obese patients having a long history of overweight as well as patients at the onset of obesity exhibit a decreased glucose-induced thermogenesis.…”

Section: Discussionmentioning

confidence: 99%

“…However reduced glucose induced thermogenesis is present at the onset of obesity in women with normal insulin plasma levels, 14 and an improvement of food-induced thermogenesis without full recovery of the defect is observed in reduced-obese subjects. 20 The activity of the SNS is under the direct tonic control of its own neurotransmitter released in physiological conditions. Noradrenaline release is controlled through a negative feedback mechanism operating through presynaptic a 2 -adrenoceptors.…”

Section: Discussionmentioning

confidence: 99%

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Glucose-induced sympathetic activity and energy expenditure during acute α2-adrenergic antagonism in obese subjects

et al. 2000

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OBJECTIVE: To determine the effect of an a 2 -adrenoceptor antagonist, idazoxan, on the sympathetic nervous system and on energy expenditure responses after an oral glucose load, in obese patients. (idazoxan acts as an indirect sympathomimetic drug through blockade of presynaptic a 2 -adrenoceptors). DESIGN: Double-blind randomized placebo-controlled cross-over study. Idazoxan (40 mg) or placebo were administered orally 90 min before a 100 g oral glucose load. SUBJECTS: Twelve long-standing obese subjects (six men and six women, age range from 24 to 45 y, body mass index range from 30.2 to 41.3 kgam 2 ). MEASUREMENTS: Energy expenditure was derived from oxygen consumption and carbon dioxide production according to indirect calorimetry. Plasma samples were obtained for plasma adrenaline and noradrenaline, glucose, non-esteri®ed fatty acid (NEFA), glycerol and insulin determinations. RESULTS: The plasma noradrenaline concentration response to the glucose load was signi®cantly higher after idazoxan than after placebo administration. The time-course of glucose load-induced thermogenesis was not signi®cantly different after administration of idazoxan nor placebo. Idazoxan administration did not modify the insulin, non-esteri®ed fatty acids or glycerol concentration responses to the glucose load. Neither heart rate nor blood pressure values were modi®ed by idazoxan when compared to placebo. However, idazoxan signi®cantly improved glucose tolerance. CONCLUSION: The a 2 -adrenergic antagonist idazoxan increases glucose-induced sympathetic activity but not energy expenditure in obese subjects. These data do not argue for the development of a a 2 AR antagonist compounds as antiobesity treatment.

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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Glucose-induced sympathetic activity and energy expenditure during acute α2-adrenergic antagonism in obese subjects

et al. 2000

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“…Diet-induced thermogenesis is considered an obligatory energy cost for digestion, absorption, transport, and other metabolic activity needed for the assimilation of nutrients. It has also been proposed as a facultative part of adaptive thermogenesis responding to excess food intake, like nonshivering thermogensis responding to cold, that involves the sympathetic nervous system and brown adipose tissues (26)(27)(28)(29)(30). Dietary fat induces the least thermogenesis (estimated at 0 Ϫ 5%), whereas protein induces the most (20 Ϫ 30%) among the energy-yielding nutrients ( 31 ).…”

Section: Discussionmentioning

confidence: 99%

Deficiency of MGAT2 increases energy expenditure without high-fat feeding and protects genetically obese mice from excessive weight gain

Nelson

Gao

Spencer

et al. 2011

Journal of Lipid Research

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for assimilation and thus exert a lower thermic effect of food (diet-induced thermogenesis) (3)(4)(5). Individuals that assimilate dietary fat effi ciently to meet their needs between meals have an advantage in enduring starvation. Thus, genes conferring this trait may be selected through evolution. During times of continuous abundance, however, individuals thrifty of energy substrates and high in metabolic effi ciency are prone to accumulating fuel surpluses in adipose and other tissues ( 6, 7 ). In humans, excessive fat accumulation is associated with metabolic diseases, including obesity, hepatic steatosis, and insulin resistance, which plague many industrialized parts of the world ( 8, 9 ).The absorption of dietary fat involves the resynthesis of digested triacylglycerol in enterocytes, mainly through a pathway catalyzed by acyl CoA:monoacylglycerol acyltransferase (MGAT) ( 10 ). Three related genes have been identifi ed that code for MGAT; among them, only Mogat2 is highly expressed in the small intestine of both mice and humans ( 11-15 ). Thus, Mogat2 probably encodes the intestinal MGAT activity, although Mogat3 is also found in the distal intestine in humans ( 14 ).Consistent with a role of MGAT2 in promoting conservation of dietary fat, mice lacking the enzyme ( Mogat2 Ϫ / Ϫ ) are resistant to obesity and other metabolic disorders induced by high-fat feeding ( 16,17 ؊ / ؊ mice expended energy and lost weight like wild-type controls. To determine whether MGAT2 defi ciency protects against obesity in the absence of high-fat feeding, we crossed Mogat2 ؊ / ؊ mice with genetically obese Agouti mice. MGAT2 defi ciency increased energy expenditure and prevented these mice from gaining excess weight. Our results suggest that MGAT2 modulates energy expenditure through multiple mechanisms, including one independent of dietary fat; these fi ndings also raise the prospect of inhibiting MGAT2 as a strategy for combating obesity and related metabolic disorders resulting from excessive calorie intake. Abbreviations: DGAT, diacylglycerol acyltransferase; MGAT, monoacylglycerol acyltransferase; RER, respiratory exchange ratio.

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“…Studies in obese adults designed to look for a decrease in the plasma catecholamine response to food Energy metabolism in obese adolescents P Tounian et al ingestion have yielded con¯icting results. 5,6,35 Whether the facultative component of food-induced thermogenesis is blunted in obese subjects remains therefore controversial, as does the possible contribution to obesity of a reduction in sympathetic nervous system activity. 36 Ours is the ®rst study of its kind in obese children.…”

Section: Discussionmentioning

confidence: 99%

Weight loss and changes in energy metabolism in massively obese adolescents

et al. 1999

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OBJECTIVE: To investigate the energy metabolism modi®cations induced by energy restriction and weight loss in massively obese adolescents. SUBJECTS: Ten massively obese girls (179 AE 31% of ideal body weight; age, 13.3 ± 16.4 y) after 2 ± 5 weeks on a lowenergy diet and 4.5 ± 11.5 months later, that is, after a substantial weight loss, and eight controls. MEASUREMENTS: Resting energy expenditure (REE) and carbohydrate-induced thermogenesis (CIT) after a sucrose load (by indirect calorimetry), plasma glucose and insulin before and after the sucrose load. RESULTS: After 2 ± 5 weeks on a low-energy diet, REE (7415 AE 904 kJad) was lower than the expected value calculated from the regression equation of REE on fat free mass in controls (P 0.005). After a 37 AE 17% reduction in excess weight, REE decreased (6405 AE 613 kJad) and remained lower than the expected value (P 0.005). At the early stages of weight loss, the area under the plasma glucose response curve was negatively correlated with CIT (r 7 0.80, P 0.01) and was higher in the six obese adolescents with low CIT than in the four with normal CIT (396 AE 52 vs 283 AE 26 mmol.l 71 .min 71 , P 0.01). After substantial weight loss, the area under the plasma insulin response curve decreased by 32% (P 0.02), and both CIT and the area under the plasma glucose response curve became similar in obese patients with low and normal CIT prior to weight loss. CONCLUSION: These results indicate that in massively obese adolescents, REE for fat-free mass is decreased at the very beginning of the process of losing weight and remains decreased as long as energy restriction and weight reduction carry on. They also indicate that the impaired CIT sometimes observed returns to normal after weight reduction suggesting that it is secondary to a decrease in glucose uptake induced by obesity-associated insulin resistance.

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Reduced thermic effect of feeding in obesity: Role of norepinephrine

Cited by 63 publications

References 13 publications

Glucose-induced sympathetic activity and energy expenditure during acute α2-adrenergic antagonism in obese subjects

Glucose-induced sympathetic activity and energy expenditure during acute α2-adrenergic antagonism in obese subjects

Deficiency of MGAT2 increases energy expenditure without high-fat feeding and protects genetically obese mice from excessive weight gain

Weight loss and changes in energy metabolism in massively obese adolescents

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