Hypothalamic stearoyl-CoA desaturase-2 (SCD2) controls whole-body energy expenditure

Exercise effectively prevents the development of obesity and obesity-related diseases such as type 2 diabetes. Capsinoids (CSNs) are capsaicin analogs found in a nonpungent pepper that increase whole body energy expenditure. Although both exercise and CSNs have antiobesity functions, the effectiveness of exercise with CSN supplementation has not yet been investigated. Here, we examined whether the beneficial effects of exercise could be further enhanced by CSN supplementation in mice. Mice were randomly assigned to four groups: 1) high-fat diet (HFD, Control), 2) HFD containing 0.3% CSNs, 3) HFD with voluntary running wheel exercise (Exercise), and 4) HFD containing 0.3% CSNs with voluntary running wheel exercise (Exercise + CSN). After 8 wk of ingestion, blood and tissues were collected and analyzed. Although CSNs significantly suppressed body weight gain under the HFD, CSN supplementation with exercise additively decreased body weight gain and fat accumulation and increased whole body energy expenditure compared with exercise alone. Exercise together with CSN supplementation robustly improved metabolic profiles, including the plasma cholesterol level. Furthermore, this combination significantly prevented diet-induced liver steatosis and decreased the size of adipocyte cells in white adipose tissue. Exercise and CSNs significantly increased cAMP levels and PKA activity in brown adipose tissue (BAT), indicating an increase of lipolysis. Moreover, they significantly activated both the oxidative phosphorylation gene program and fatty acid oxidation in skeletal muscle. These results indicate that CSNs efficiently promote the antiobesity effect of exercise, in part by increasing energy expenditure via the activation of fat oxidation in skeletal muscle and lipolysis in BAT.

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Daily Ingestion of Grains of Paradise (Aframomum melegueta) Extract Increases Whole-Body Energy Expenditure and Decreases Visceral Fat in Humans

Journal of Nutritional Science and Vitaminology ◽

10.3177/jnsv.60.22 ◽

2014 ◽

Vol 60 (1) ◽

pp. 22-27 ◽

Cited By ~ 14

Author(s):

Jun SUGITA ◽

Takeshi YONESHIRO ◽

Yuuki SUGISHIMA ◽

Takeshi IKEMOTO ◽

Hideyo UCHIWA ◽

...

Keyword(s):

Energy Expenditure ◽

Visceral Fat ◽

Whole Body ◽

Daily Ingestion ◽

Body Energy

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Hepatocyte-specific Hepatocyte Nuclear Factor 4 alpha (HNF4) deletion decreases resting energy expenditure by disrupting lipid and carbohydrate homeostasis

Gene Expression ◽

10.3727/105221621x16153933463538 ◽

2021 ◽

Author(s):

Ian Huck ◽

E. Matthew Morris ◽

John Thyfault ◽

Udayan Apte

Keyword(s):

Energy Expenditure ◽

Energy Homeostasis ◽

Energy Utilization ◽

Lipid Absorption ◽

Whole Body ◽

Positive Energy ◽

Nuclear Factor ◽

Hepatocyte Nuclear Factor ◽

Hepatocyte Nuclear Factor 4 ◽

Body Energy

Hepatocyte Nuclear Factor 4 alpha (HNF4α) is required for hepatocyte differentiation and regulates expression of genes involved in lipid and carbohydrate metabolism including those that control VLDL secretion and gluconeogenesis. Whereas previous studies have focused on specific genes regulated by HNF4α in metabolism, its overall role in whole body energy utilization has not been studied. In this study, we used indirect calorimetry to determine the effect of hepatocyte-specific HNF4α deletion (HNF4α-KO) in mice on whole body energy expenditure (EE) and substrate utilization in fed, fasted, and high fat diet (HFD) conditions. HNF4α-KO had reduced resting EE during fed conditions and higher rates of carbohydrate oxidation with fasting. HNF4α-KO mice exhibited decreased body mass caused by fat mass depletion despite no change in energy intake and evidence of positive energy balance. HNF4α-KO mice were able to upregulate lipid oxidation during HFD suggesting that their metabolic flexibility was intact. However, only hepatocyte specific HNF4α-KO mice exhibited significant reduction in basal metabolic rate and spontaneous activity during HFD. Consistent with previous studies, hepatic gene expression in HNF4α-KO supports decreased gluconeogenesis and decreased VLDL export and hepatic Beta-oxidation in HNF4α-KO livers across all feeding conditions. Together, our data suggest deletion of hepatic HNF4α increases dependence on dietary carbohydrates and endogenous lipids for energy during fed and fasted conditions by inhibiting hepatic gluconeogenesis, hepatic lipid export, and intestinal lipid absorption resulting in decreased whole body energy expenditure. These data clarify the role of hepatic HNF4α on systemic metabolism and energy homeostasis.

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Anxious to lose weight

Science Translational Medicine ◽

10.1126/scitranslmed.aaw5329 ◽

2019 ◽

Vol 11 (480) ◽

pp. eaaw5329

Author(s):

Riekelt Houtkooper

Keyword(s):

Weight Gain ◽

Energy Expenditure ◽

High Fat Diet ◽

Whole Body ◽

High Fat ◽

Body Energy

Anxiety leads to increased whole-body energy expenditure and thermogenesis in mice, preventing weight gain upon high-fat diet feeding.

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The Influence of Shc Proteins and Aging on Whole Body Energy Expenditure and Substrate Utilization in Mice

PLoS ONE ◽

10.1371/journal.pone.0048790 ◽

2012 ◽

Vol 7 (11) ◽

pp. e48790 ◽

Cited By ~ 4

Author(s):

Jennifer H. Stern ◽

Kyoungmi Kim ◽

Jon J. Ramsey

Keyword(s):

Energy Expenditure ◽

Substrate Utilization ◽

Whole Body ◽

Body Energy

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Direct and indirect calorimetry of lactate oxidation: implications for whole-body energy expenditure

Journal of Sports Sciences ◽

10.1080/02640410410001716760 ◽

2005 ◽

Vol 23 (1) ◽

pp. 15-19 ◽

Cited By ~ 19

Author(s):

Christopher Scott ◽

Richard Kemp

Keyword(s):

Energy Expenditure ◽

Indirect Calorimetry ◽

Whole Body ◽

Lactate Oxidation ◽

Body Energy

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Role of alpha- and beta-adrenoceptors in sympathetically mediated thermogenesis

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1993.264.1.e11 ◽

1993 ◽

Vol 264 (1) ◽

pp. E11-E17 ◽

Cited By ~ 8

Author(s):

E. E. Blaak ◽

M. A. van Baak ◽

K. P. Kempen ◽

W. H. Saris

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Energy Expenditure ◽

Whole Body ◽

Healthy Male ◽

Beta Adrenoceptor ◽

Beta 2 ◽

Body Energy ◽

Stimulation Of

This study was intended to investigate the role of alpha- and beta-adrenoceptor populations in the sympathetically mediated thermogenesis in healthy lean males. In the first study, the beta 1-, beta 2-, and beta 3-agonist isoprenaline was infused in increasing doses with and without simultaneous infusion of the beta 1-blocker atenolol (Iso and Iso+AT, respectively). There was an increase in whole body energy expenditure (EE) after infusing Iso+AT (P < 0.001) and an almost twofold higher increase after infusion of Iso only (P < 0.001). Stimulation of the beta 2-adrenoceptors by a specific agonist (salbutamol) resulted in a significant increase in EE (P < 0.001). The effect of stimulation of alpha 1-adrenoceptors on EE was measured by infusing increasing doses of the alpha 1-agonist phenylephrine. EE did not change, whereas blood pressure (BP) increased (P < 0.001) and heart rate decreased (P < 0.01). In addition to this study, the alpha 1-, alpha 2-, beta 1-, beta 2-, and beta 3-agonists norepinephrine and epinephrine were infused with simultaneous infusion of the beta 1- and beta 2-blocker propranolol. In both studies, there was no effect on EE, whereas BP increased (P < 0.01). In conclusion, in healthy male lean volunteers both beta 1- and beta 2-adrenoceptors are involved in the sympathetically mediated thermogenesis, whereas the alpha 1-, alpha 2-, and beta 3-adrenoceptors do not play a role.

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