scholarly journals An insulin-stimulated proteolytic mechanism links energy expenditure with glucose uptake

2019 ◽  
Author(s):  
Estifanos N. Habtemichael ◽  
Don T. Li ◽  
João Paulo Camporez ◽  
Xavier O. Westergaard ◽  
Chloe I. Sales ◽  
...  
Keyword(s):  
Energy Expenditure ◽  
Glucose Uptake ◽  
Genetic Manipulation ◽  
Degradation Mechanism ◽  
Cleavage Product ◽  
Whole Body ◽  
Thermic Effect Of Food ◽  
Endoproteolytic Cleavage ◽  
Effect Of Food ◽  
Body Energy

SummaryMechanisms to coordinately regulate energy expenditure and glucose uptake into muscle and fat cells are not well described. Insulin stimulates glucose uptake in part by causing site-specific endoproteolytic cleavage of TUG, which mobilizes GLUT4 glucose transporters to the cell surface. Here, we show that the TUG C-terminal cleavage product enters the nucleus, binds the transcriptional regulators PGC-1α and PPARγ, and increases oxidative metabolism and thermogenic protein expression. Muscle-specific genetic manipulation of this pathway impacts whole-body energy expenditure, independent of glucose uptake. The PPARγ2 Pro12Ala polymorphism, which reduces diabetes risk, enhances TUG binding. The TUG cleavage product stabilizes PGC-1α and is itself susceptible to an Ate1 arginyltransferase -dependent degradation mechanism; binding of the TUG product confers Ate1-dependent stability upon PGC-1α. We conclude that TUG cleavage coordinates energy expenditure with glucose uptake, that this pathway may contribute to the thermic effect of food, and that its attenuation may be important in obesity.

Adipocyte-specific mTORC2 deficiency impairs BAT and iWAT thermogenic capacity without affecting glucose uptake and energy expenditure in cold-acclimated mice

2021 ◽  
Author(s):  
Erique Castro ◽  
Thayna S Vieira ◽  
Tiago E. Oliveira ◽  
Milene Ortiz-Silva ◽  
Maynara L Andrade ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Expenditure ◽  
Glucose Uptake ◽  
Residual Activity ◽  
De Novo Lipogenesis ◽  
Whole Body ◽  
Mrna Levels ◽  
Brown Adipose ◽  
Body Energy ◽  
Thermogenic Capacity

Deletion of mTORC2 essential component Rictor by a Cre recombinase under control of the broad, non-adipocyte specific aP2/FABP4 promoter impairs thermoregulation and brown adipose tissue (BAT) glucose uptake upon acute cold exposure. We investigated herein whether adipocyte-specific mTORC2 deficiency affects BAT and inguinal white adipose tissue (iWAT) signaling, metabolism and thermogenesis in cold-acclimated mice. For this, 8-weeks old male mice bearing Rictor deletion and therefore mTORC2 deficiency in adipocytes (adiponectin-Cre) and littermates controls were either kept at thermoneutrality (30 ± 1ºC) or cold-acclimated (10 ± 1ºC) for 14 days and evaluated for BAT and iWAT signaling, metabolism and thermogenesis. Cold acclimation inhibited mTORC2 in BAT and iWAT, but its residual activity is still required for the cold-induced increases in BAT adipocyte number, total UCP-1 content and mRNA levels of proliferation markers Ki67 and cyclin 1D and de novo lipogenesis enzymes ATP-citrate lyase and acetyl-CoA carboxylase. In iWAT, mTORC2 residual activity is partially required for the cold-induced increases in multilocular adipocytes, mitochondrial mass and UCP-1 content. Conversely, BAT mTORC1 activity and BAT and iWAT glucose uptake were upregulated by cold independently of mTORC2. Noteworthy, the impairment in BAT and iWAT total UCP-1 content and thermogenic capacity induced by adipocyte mTORC2 deficiency had no major impact on whole-body energy expenditure in cold-acclimated mice due to a compensatory activation of muscle shivering. In conclusion, adipocyte mTORC2 deficiency impairs, through different mechanisms, BAT and iWAT total UCP-1 content and thermogenic capacity in cold-acclimated mice, without affecting glucose uptake and whole-body energy expenditure.

Role of thermogenesis in the regulation of energy balance in relation to obesity

1989 ◽  
Vol 67 (4) ◽  
pp. 394-401 ◽  
Author(s):  
Jean Himms-Hagen
Keyword(s):  
Adipose Tissue ◽  
Energy Balance ◽  
Energy Expenditure ◽  
Brown Adipose Tissue ◽  
Thermal Balance ◽  
Prominent Feature ◽  
Thermic Effect Of Food ◽  
Brown Adipose ◽  
Effect Of Food ◽  
Thermic Effect

Obligatory thermogenesis is a necessary accompaniment of all metabolic processes involved in maintenance of the body in the living state, and occurs in ail organs. It includes energy expenditure involved in ingesting, digesting, and processing food (thermic effect of food (TEF)). At certain life stages extra energy expenditure for growth, pregnancy, or lactation would also be obligatory. Facultative thermogenesis is superimposed on obligatory thermogenesis and can be rapidly switched on and rapidly suppressed by the nervous system. Facultative thermogenesis is important in both thermal balance, in which control of thermoregulatory thermogenesis (shivering in muscle, nonshivering in brown adipose tissue (BAT)) balances neural control of heat loss mechanisms, and in energy balance, in which control of facultative thermogenesis (exercise-induced in muscle, diet-induced thermogenesis (DIT) in BAT) balances control of energy intake. Thermal balance (i.e., body temperature) is much more stringently controlled than energy balance (i.e., body energy stores). Reduced energy expenditure for thermogenesis is important in two types of obesity in laboratory animals. In the first type, deficient DIT in BAT is a prominent feature of altered energy balance. It may or may not be associated with hyperphagia. In a second type, reduced cold-induced thermogenesis in BAT as well as in other organs is a prominent feature of altered thermal balance. This in turn results in altered energy balance and obesity, exacerbated in some examples by hyperphagia. In some of the hyperphagic obese animals it is likely that the exaggerated obligatory thermic effect of food so alters thermal balance that BAT thermogenesis is suppressed. In all obese animals, deficient hypothalamic control of facultative thermogenesis and (or) food intake is implicated.Key words: thermogenesis, brown adipose tissue, energy balance, obesity, cold, thermoregulation, diet.

Thermogenic response to epinephrine in the forearm and abdominal subcutaneous adipose tissue

1992 ◽  
Vol 263 (5) ◽  
pp. E850-E855 ◽  
Author(s):  
L. Simonsen ◽  
J. Bulow ◽  
J. Madsen ◽  
N. J. Christensen
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Energy Expenditure ◽  
Oxygen Uptake ◽  
Glucose Uptake ◽  
Subcutaneous Adipose Tissue ◽  
Whole Body ◽  
Epinephrine Infusion ◽  
Basal Period ◽  
Subcutaneous Adipose

Whole body energy expenditure, thermogenic and metabolic changes in the forearm, and intercellular glucose concentrations in subcutaneous adipose tissue on the abdomen determined by microdialysis were measured during epinephrine infusion in healthy subjects. After a control period, epinephrine was infused at rates of 0.2 and 0.4 nmol.kg-1 x min-1. Whole body resting energy expenditure was 4.36 +/- 0.56 (SD) kJ/min. Energy expenditure increased to 5.14 +/- 0.74 and 5.46 +/- 0.79 kJ/min, respectively (P < 0.001), during the epinephrine infusions. Respiratory exchange ratio was 0.80 +/- 0.04 in the resting state and did not change. Local forearm oxygen uptake was 3.9 +/- 1.3 mumol.100 g-1 x min-1 in the basal period. During epinephrine infusion, it increased to 5.8 +/- 2.1 (P < 0.03) and 7.5 +/- 2.3 mumol.100 g-1 x min-1 (P < 0.001). Local forearm glucose uptake was 0.160 +/- 0.105 mumol.100 g-1 x min-1 and increased to 0.586 +/- 0.445 and 0.760 +/- 0.534 mumol.100 g-1 x min-1 (P < 0.025). The intercellular glucose concentration in the subcutaneous adipose tissue on the abdomen was equal to the arterial concentration in the basal period but did not increase as much during infusion of epinephrine, indicating glucose uptake in adipose tissue in this condition. If it is assumed that forearm skeletal muscle is representative for the average skeletal muscle, it can be calculated that on average 40% of the enhanced whole body oxygen uptake induced by infusion of epinephrine is taking place in skeletal muscle. It is proposed that adipose tissue may contribute to epinephrine-induced thermogenesis.

Intraduodenal infusion of α-ketoglutarate decreases whole body energy expenditure in growing pigs

2006 ◽  
Vol 25 (3) ◽  
pp. 489-496 ◽  
Author(s):  
Peter Junghans ◽  
Michael Derno ◽  
Stefan Pierzynowski ◽  
Ulf Hennig ◽  
Paul Eberhard Rudolph ◽  
...  
Keyword(s):  
Energy Expenditure ◽  
Growing Pigs ◽  
Whole Body ◽  
Intraduodenal Infusion ◽  
Body Energy

Thermic effect of food in hypothyroid rats

1996 ◽  
Vol 148 (1) ◽  
pp. 167-174 ◽  
Author(s):  
S Iossa ◽  
L Lionetti ◽  
M P Mollica ◽  
A Barletta ◽  
G Liverini
Keyword(s):  
Energy Expenditure ◽  
Insulin Release ◽  
Adrenergic Response ◽  
Thermic Effect Of Food ◽  
Effect Of Food ◽  
Postprandial Thermogenesis ◽  
Thermic Effect ◽  
Thermogenic Response

Abstract The regulatory and obligatory components of cephalic and gastrointestinal phases of the thermic effect of food (TEF) were measured in control and hypothyroid rats. A significant decrease (P<0·05) in regulatory and obligatory components of cephalic and gastrointestinal TEF, after either a control or energy-dense meal, was found in hypothyroid rats compared with control rats. Our findings indicate that hypothyroidism is associated with a decreased thermogenic response to food which contributes to the reduced energy expenditure of hypothyroid rats. Our results also suggest that tri-iodothyronine is involved in the regulation of postprandial thermogenesis directly as well as through its influence on β-adrenergic response and insulin release. Journal of Endocrinology (1996) 148, 167–174

scholarly journals A combination of exercise and capsinoid supplementation additively suppresses diet-induced obesity by increasing energy expenditure in mice

2015 ◽  
Vol 308 (4) ◽  
pp. E315-E323 ◽  
Author(s):  
Kana Ohyama ◽  
Yoshihito Nogusa ◽  
Katsuya Suzuki ◽  
Kosaku Shinoda ◽  
Shingo Kajimura ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Energy Expenditure ◽  
Body Weight Gain ◽  
Whole Body ◽  
Voluntary Running ◽  
Running Wheel Exercise ◽  
Body Energy

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.

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

2014 ◽  
Vol 60 (1) ◽  
pp. 22-27 ◽  
Author(s):  
Jun SUGITA ◽  
Takeshi YONESHIRO ◽  
Yuuki SUGISHIMA ◽  
Takeshi IKEMOTO ◽  
Hideyo UCHIWA ◽  
...  
Keyword(s):  
Energy Expenditure ◽  
Visceral Fat ◽  
Whole Body ◽  
Daily Ingestion ◽  
Body Energy

Energy expenditure during carbohydrate overfeeding in obese and nonobese adolescents

1989 ◽  
Vol 256 (3) ◽  
pp. E357-E367 ◽  
Author(s):  
L. G. Bandini ◽  
D. A. Schoeller ◽  
J. Edwards ◽  
V. R. Young ◽  
S. H. Oh ◽  
...  
Keyword(s):  
Energy Expenditure ◽  
Urinary Excretion ◽  
Weight Maintenance ◽  
Blood Levels ◽  
Obese Adolescents ◽  
Thermic Effect Of Food ◽  
Before And After ◽  
Total Daily Energy Expenditure ◽  
Effect Of Food ◽  
Doubly Labeled Water Method

Basal metabolic rate (BMR), thermic effect of food (TEF), and total daily energy expenditure (TDEE) were measured in six nonobese and seven obese adolescents during periods of weight maintenance and 2 wk of carbohydrate overfeeding. BMR and TEF were measured by indirect calorimetry and TDEE by the doubly labeled water method. Fasting blood levels of insulin, thyroid, and norepinephrine (NE) and urinary excretion of NE and 4-hydroxy-3-methoxymandelic acid (VMA) were measured before and after overfeeding. Energy intake was 1.61 X BMR during maintenance and 2.45 X BMR during overfeeding. BMR increased comparably in both groups during overfeeding (obese, 7.9 +/- 1.2%, nonobese, 8.6 +/- 1.9%). TEF was similar and did not change significantly during overfeeding (maintenance: obese, 9.4 +/- 0.6%; nonobese, 9.8 +/- 0.4% vs. overfeeding: obese, 8.6 +/- 0.3%; nonobese, 9.2 +/- 0.7%). TDEE did not differ significantly between obese and nonobese. Increases in insulin and 3,5,3'-triiodothyronine levels were significant but did not differ between the two groups. Plasma NE and urinary excretion of VMA and NE did not increase during overfeeding. The thermogenic response to food or to overfeeding does not appear reduced in obese adolescents, nor does facultative thermogenesis appear to be a significant factor in weight maintenance in adolescents.

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