Involvement of insulin in the acute thermogenic responses to food and nonmetabolizable substances

Rothwell, Nancy J.; Stock, Michael J.; Warwick, Barry P.

doi:10.1016/0026-0495(85)90058-7

Cited by 15 publications

(3 citation statements)

References 9 publications

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“…Insulin may play a role in the central stimulation of thermogenesis in BAT via activation of the sympathetic nervous system [20,21], but it also has direct effects on the tissue. In addition to activating pyruvate dehydrogenase and acetyl-CoA carboxylase [ 14,151, insulin stimulates glucose uptake by BAT [22], and the tissue may be quantitatively important in the removal of glucose from blood [22-261.…”

Section: Resultsmentioning

confidence: 99%

Effects of ciglitazone on insulin resistance and thermogenic responsiveness to acute cold in brown adipose tissue of genetically obese (ob/ob) mice

Mercer

Trayhurn

1986

FEBS Letters

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Genetically obese (ob/ob) mice develop a marked insulin resistance in brown adipose tissue soon after weaning, and this is paralleled by a fall in the acute activation of the mitochondrial proton conductance pathway in the tissue on cold exposure. Treatment of ob/ob mice with ciglitazone, a new oral hypoglycaemic, led to a restoration of insulin sensitivity in brown adipose tissue. The amelioration of insulin resistance was accompanied by a normalization of the acute, cold‐induced increase in mitochondrial GDP binding. These results support the hypothesis that the development of insulin resistance in brown adipose tissue is an important factor in the impaired thermogenic responsiveness of obese mice.

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Section: Resultsmentioning

confidence: 99%

Effects of ciglitazone on insulin resistance and thermogenic responsiveness to acute cold in brown adipose tissue of genetically obese (ob/ob) mice

Mercer

Trayhurn

1986

FEBS Letters

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“…Insulin has been implicated in the thermic effect of carbohydrate feeding in rats (Rothwell et al 1985), but not in man (Christin et al 1986). It may also increase 0, consumption in skeletal muscle after exercise (Balon et al 1984).…”

Section: Discussionmentioning

confidence: 99%

Energy balance in rats given chronic hormone treatment

Woodward

Emery

1989

Br J Nutr

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1. Sprague-Dawley rats were injected for 16 d with long-acting insulin, and energy balance was calculated using the comparative carcass technique. Two experiments were carried out with females (starting weights 150 and 90 g respectively), and one with males (starting weight 150 8). In a fourth experiment, cytochrome c oxidasc (EC 1 .9.3.1) activity was measured as an indicator of the capacity for substrate oxidation. 2.Insulin increased weight gain by up to 57% ( P < 0.01 for all studies). Metabolizable energy intake (kJ/d) was also consistently higher in the treated groups, by up to 34% (P < 0.01 for all studies). The excess weight gained by the insulin-treated rats was predominantly due to fat deposition.3. Energy expenditure, calculated as the difference between metabolizable intake and carcass energy gain. was expressed on a whole-body basis, or relative to either metabolic body size (kg body-weight"75) or fat-free mass. Insulin consistently raised energy expenditure, regardless of the method of expression, but this change reached statistical significance in only two of the nine comparisons.4. Cytochrome c oxidase activity was not affected by insulin treatment in either interscapular brown adipose tissue or gastrocnemius muscle. In liver, total enzyme activity (U/tissue) was increased from 2928 (SF 162) in the controls to 3940 (SE 294) in the treated group ( P i 002), but specific activity (U/mg protein) was unchanged.5. It is concluded that, despite causing substantial hyperphagia, insulin treatment only slightly increases energy expenditure in rats. The costs of increased tissue deposition may account for this change.

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“…One possible mediator of the enhanced thermic effect of food in the postexercise state is insulin, because the themic effect of ingested carbohydrate is lost or diminished in streptozotocininduced diabetic rats (Rothwell and Stock 1981), in rats in which insulin secretion is blocked by diazoxide (Rothwell et al 1985), armd in obese diabetic insulin-resistant humans (Golay et al 1983). The themic effect of insulin has, in great measure, been attributed to its ability to enhance glucose storage in skeletal muscle (Ravussin and Bogardus 1982;Ravussin et al 1983).…”

Section: Thermic Eflect Of Eatingmentioning

confidence: 99%

Exercise and postexercise energy expenditure in growing pigs

Petley

Bayley²

1988

Can. J. Physiol. Pharmacol.

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Young pigs (ca. 10 kg) were trained to run on a motor-driven treadmill for 1 h each day. After a 2-week training period the gas exchange of exercised and control animals was measured using an open circuit, indirect calorimeter. The exercised pigs ran for 2 h in the calorimeter, and then rested for 2 h. They received a day's allocation of feed and remained in the calorimeter for a total of 23 h. The total heat production of the exercised pigs was 523 kJ/kg, compared with 433 kJ/kg of the controls. Monitoring the heat production throughout the 23-h period showed that only 43% of the extra heat dissipated by the exercised pigs was lost during the 2 h of exercise, with a higher rate of heat production for the remaining 21 h accounting for the 57% of the extra energy dissipated as heat. The results suggest that exercise increases energy expenditure well beyond the time devoted to the activity itself.

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Involvement of insulin in the acute thermogenic responses to food and nonmetabolizable substances

Cited by 15 publications

References 9 publications

Effects of ciglitazone on insulin resistance and thermogenic responsiveness to acute cold in brown adipose tissue of genetically obese (ob/ob) mice

Effects of ciglitazone on insulin resistance and thermogenic responsiveness to acute cold in brown adipose tissue of genetically obese (ob/ob) mice

Energy balance in rats given chronic hormone treatment

Exercise and postexercise energy expenditure in growing pigs

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