Mechanisms of thermogenesis induced by low protein diets

Rothwell, Nancy J.; Stock, Michael J.; Tyzbir, Robert S.

doi:10.1016/0026-0495(83)90190-7

Cited by 121 publications

(82 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, it is noteworthy that the hyperphagia, augmented thermogenesis and reduction in weight gain with our 0P and 5P, and the hyperphagia with 10P, is consistent with numerous other studies reporting similar findings in normal lean Sprague Dawley rats [7][8][9]19,21,55,56 . Although, the thermogenic activity of brown adipose tissue to dietary stimuli is often weak in obese animals 57 , the augmented thermogenesis with dietary protein restriction in our OP-CD rats suggests that effects of low protein diets on energy balance might be conserved in both lean and obese phenotypes.…”

Section: Discussionsupporting

confidence: 93%

“…Despite an initial increase in energy expenditure, this effect did not persist in the 0P likely due to the sustained anorexia and weight loss. Previous studies have shown that an increased sympathetic influx to BAT is required for the thermogenic effects of low protein diets [19][20][21][22][23] . In the present study, using propranolol, a β -AR antagonist, we demonstrate that energy expenditure was dose-dependently attenuated in animals fed low protein diets with maximal attenuation in protein deprived rats.…”

Section: Discussionmentioning

confidence: 99%

“…Low protein diets also enhance energy expenditure in rodents 17,[19][20][21][22] , however, the underlying mechanisms are poorly understood. Potential mechanisms include increased sympathetic flux via β -adrenergic receptor (β -AR) signaling to brown adipose tissue (BAT) with consequent upregulation of mitochondrial uncoupling protein-1 (UCP1) expression 19,[21][22][23] , as well as increased fibroblast growth factor-21 (FGF21) mediated thermogenesis 17 . However, the relative importance of these mechanisms, and whether gut-derived signals are associated with low protein induced hyperphagia and thermogenesis, are largely unknown.…”

mentioning

confidence: 99%

“…These include imbalances in plasma and brain amino acid concentrations in rats [15][16][17] , modulation of energy sensors in the hypothalamus and anterior piriform cortex in rats 18 , and increased activity in the reward areas such as the orbitofrontal cortex and striatum in humans 11 . Low protein diets also enhance energy expenditure in rodents 17,[19][20][21][22] , however, the underlying mechanisms are poorly understood. Potential mechanisms include increased sympathetic flux via β -adrenergic receptor (β -AR) signaling to brown adipose tissue (BAT) with consequent upregulation of mitochondrial uncoupling protein-1 (UCP1) expression 19,[21][22][23] , as well as increased fibroblast growth factor-21 (FGF21) mediated thermogenesis Scientific RepoRts | 6:25145 | DOI: 10.1038/srep25145…”

mentioning

confidence: 99%

See 3 more Smart Citations

0476 Low protein diets produce divergent effects on energy balance

Zapata

Pezeshki

Singh

et al. 2016

Journal of Animal Science

View full text Add to dashboard Cite

Diets deficient in protein often increase food consumption, body weight and fat mass; however, the underlying mechanisms remain poorly understood. We compared the effects of diets varying in protein concentrations on energy balance in obesity-prone rats. We demonstrate that protein-free (0% protein calories) diets decreased energy intake and increased energy expenditure, very low protein (5% protein) diets increased energy intake and expenditure, whereas moderately low protein (10% protein) diets increased energy intake without altering expenditure, relative to control diet (15% protein). These diet-induced alterations in energy expenditure are in part mediated through enhanced serotonergic and β-adrenergic signaling coupled with upregulation of key thermogenic markers in brown fat and skeletal muscle. The protein-free and very low protein diets decreased plasma concentrations of multiple essential amino acids, anorexigenic and metabolic hormones, but these diets increased the tissue expression and plasma concentrations of fibroblast growth factor-21. Protein-free and very low protein diets induced fatty liver, reduced energy digestibility, and decreased lean mass and body weight that persisted beyond the restriction period. In contrast, moderately low protein diets promoted gain in body weight and adiposity following the period of protein restriction. Together, our findings demonstrate that low protein diets produce divergent effects on energy balance.The consumption of protein triggers adaptive responses in ingestive behavior, energy expenditure and metabolism that are under homeostatic controls. The 'protein leverage' hypothesis posits that protein intake is tightly regulated in several species including rats, mice and humans, which consume to acquire their required protein rather than meet requirements for fats and carbohydrates [1][2][3] . An increase in dietary protein density would decrease intake of carbohydrates and fats with consequent reduction in energy intake. There is substantial evidence that high protein diets promote satiety, weight loss and improve glycemic control 4,5 . A corollary to this hypothesis is that a reduction in the dietary protein concentration would increase total energy intake, due to overconsumption of carbohydrates and fat, in an effort to meet protein requirements. Consistent with this, moderately protein deficient diets were found to produce hyperphagia in rodents 6-9 and in some 1,10,11 but not all human studies 12,13 , whereas, severe protein restriction below a certain threshold leads to a reduction in food intake in rodents 9,14 . However, little is known of the underlying mechanisms by which moderate protein deficiency elicits such behavioural and metabolic adaptations and promotes positive energy balance with consequent predisposition to obesity and other metabolic disorders.The hyperphagic effects of moderately low protein diets are purported to be through multiple mechanisms. These include imbalances in plasma and brain amino acid concentrations in rats [15][16][17] ,...

show abstract

Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

0476 Low protein diets produce divergent effects on energy balance

Zapata

Pezeshki

Singh

et al. 2016

Journal of Animal Science

View full text Add to dashboard Cite

show abstract

“…In particular, a large increase in the activity of brown adipose tissue has been described (4)(5)(6). In keeping with this picture, one of the hormones most directly involved in energy dissipation, norepinephrine (NE), is elevated in rats fed low-protein diets (7,8).…”

Section: Introductionmentioning

confidence: 93%

Increase in skeletal muscle protein content by the ß-2 selective adrenergic agonist clenbuterol exacerbates hypoalbuminemia in rats fed a low-protein diet

Sawaya

Lunn

1998

Braz J Med Biol Res

View full text Add to dashboard Cite

This investigation examined how the nutritional status of rats fed a low-protein diet was affected when the animals were treated with the ß-2 selective agonist clenbuterol (CL). Males (4 weeks old) from an inbred, specific-pathogen-free strain of hooded rats maintained at the Dunn Nutritional Laboratory were used in the experiments (N = 6 rats per group). CL treatment (Ventipulmin, Boehringer-Ingelheim Ltd., 3.2 mg/kg diet for 2 weeks) caused an exacerbation of the symptoms associated with protein deficiency in rats. Plasma albumin concentrations, already low in rats fed a low-protein diet (group A), were further reduced in CL rats (A = 25.05 ± 0.31 vs CL = 23.64 ± 0.30 g/l, P<0.05). Total liver protein decreased below the level seen in either pair-fed animals (group P) or animals with free access to the low-protein diet (A = 736.56 ± 26 vs CL = 535.41 ± 54 mg, P<0.05), whereas gastrocnemius muscle protein was higher than the values normally described for control (C) animals (C = 210.88 ± 3.2 vs CL = 227.14 ± 1.7 mg/g, P<0.05). Clenbuterol-treated rats also showed a reduction in growth when compared to P rats (P = 3.2 ± 1.1 vs CL = -10.2 ± 1.9 g, P<0.05). This was associated with a marked decrease in fat stores (P = 5.35 ± 0.81 vs CL = 2.02 ± 0.16 g, P<0.05). Brown adipose tissue (BAT) cytochrome oxidase activity, although slightly lower than in P rats (P = 469.96 ± 16.20 vs CL = 414.48 ± 11.32 U/BAT x kg body weight, P<0.05), was still much higher than in control rats (C = 159.55 ± 11.54 vs CL = 414.48 ± 11.32 U/BAT x kg body weight, P<0.05). The present findings support the hypothesis that an increased muscle protein content due to clenbuterol stimulation worsened amino acid availability to the liver and further reduced albumin synthesis causing exacerbation of hypoalbuminemia in rats fed a low-protein diet. Correspondence

show abstract

Central Nervous System Regulation of Brown Adipose Tissue

Morrison

Madden

2014

Comprehensive Physiology

124

103

View full text Add to dashboard Cite

Thermogenesis, the production of heat energy, in brown adipose tissue is a significant component of the homeostatic repertoire to maintain body temperature during the challenge of low environmental temperature in many species from mouse to man and plays a key role in elevating body temperature during the febrile response to infection. The sympathetic neural outflow determining brown adipose tissue (BAT) thermogenesis is regulated by neural networks in the CNS which increase BAT sympathetic nerve activity in response to cutaneous and deep body thermoreceptor signals. Many behavioral states, including wakefulness, immunologic responses, and stress, are characterized by elevations in core body temperature to which central command-driven BAT activation makes a significant contribution. Since energy consumption during BAT thermogenesis involves oxidation of lipid and glucose fuel molecules, the CNS network driving cold-defensive and behavioral state-related BAT activation is strongly influenced by signals reflecting the short and long-term availability of the fuel molecules essential for BAT metabolism and, in turn, the regulation of BAT thermogenesis in response to metabolic signals can contribute to energy balance, regulation of body adipose stores and glucose utilization. This review summarizes our understanding of the functional organization and neurochemical influences within the CNS networks that modulate the level of BAT sympathetic nerve activity to produce the thermoregulatory and metabolic alterations in BAT thermogenesis and BAT energy expenditure that contribute to overall energy homeostasis and the autonomic support of behavior.

show abstract

Mechanisms of thermogenesis induced by low protein diets

Cited by 121 publications

References 20 publications

0476 Low protein diets produce divergent effects on energy balance

0476 Low protein diets produce divergent effects on energy balance

Increase in skeletal muscle protein content by the ß-2 selective adrenergic agonist clenbuterol exacerbates hypoalbuminemia in rats fed a low-protein diet

Central Nervous System Regulation of Brown Adipose Tissue

Contact Info

Product

Resources

About