Food intake, resting metabolic rate and diet-induced thermogenesis of young Chinese females in the luteal and follicular phases of the menstrual cycle

1998 ◽  
Author(s):  
Bo-yee Tsang
Keyword(s):  
Menstrual Cycle ◽  
Food Intake ◽  
Metabolic Rate ◽  
Resting Metabolic Rate ◽  
Diet Induced Thermogenesis

Abstract 010: The Role of Angiotensin AT 1A Receptors in Leptin-sensitive Cells in Resting Metabolic Rate Control

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Kristin E Claflin ◽  
Justin L Grobe
Keyword(s):  
Metabolic Rate ◽  
Rate Control ◽  
Leptin Receptor ◽  
Resting Metabolic Rate ◽  
Critical Role ◽  
Renin Angiotensin System ◽  
Chow Diet ◽  
Brown Adipose ◽  
Diet Induced Thermogenesis ◽  
The Brain

The brain renin-angiotensin system (RAS) and leptin contribute to the control of resting metabolic rate (RMR) and their receptors are co-expressed in areas of the brain critical for metabolic control; thus angiotensin and leptin may interact within the brain to regulate RMR and obesity. Inhibition of the brain RAS attenuates sympathetic nerve activity (SNA) responses to leptin, leading us to hypothesize that the brain RAS mediates the RMR effects of leptin. Mice lacking angiotensin AT 1A receptors in leptin receptor-expressing cells (ObRb-Cre x AT 1A flox/flox ; “KO”) exhibited normal body weight (15 weeks of age: control n=28, 26.0 ± 0.7, vs KO n=35, 25.8 ± 0.6 g), food intake (control n=12, 3.1 ± 0.15, vs KO n=15, 3.4 ± 0.14 g) and RMR (control n=13, 0.15 ± 0.004, vs KO n=15, 0.16 ± 0.006 kcal/hr) on standard chow diet. Brown adipose SNA responses to acute leptin injection, however, were completely attenuated in KO mice. When maintained on a 45% high fat diet (HFD), KO mice gained significantly more fat mass (control n=35, 5.6 ± 0.4, vs KO n=31, 7.4 ± 0.5 g, P<0.05) and body mass (control, 27.4 ± 0.6, vs KO, 29.6 ± 0.6 g, P<0.05) due to a loss of diet-induced thermogenesis (control n=22, 0.18 ± 0.008, vs. KO n=12, 0.16 ± 0.004 kcal/hr, P<0.05). KO mice exhibited attenuated hypothalamic proopiomelanocortin (POMC) gene expression and partially attenuated RMR responses to alpha-melanocyte stimulating hormone (αMSH; control n=3, 0.25 ± 0.01, vs KO n=7, 0.2 ± 0.01 kcal/hr, P<0.05) indicating that the interaction between leptin and AT 1A modulates both αMSH production and action. To localize the site of the brain RAS-leptin interaction, we developed novel multi-transgenic mouse models which expresses GFP via the AT 1A promoter (NZ44, from GenSat) and/or conditional activation of a tdTomato reporter (ROSA-stop flox -tdTomato) in cells expressing the leptin receptor (ObRb-Cre) or agouti-related peptide (AgRP-Cre). Immunohistochemical staining of adrenocorticotropin in brain tissue from NZ44 mice revealed no localization of AT 1A to POMC neurons; in contrast, AT 1A was strongly localized with AgRP promoter activity. Taken together, these data support a critical role for angiotensin AT 1A receptors on AgRP neurons in the arcuate nucleus in resting metabolic rate control.

scholarly journals Alcohol and its acute effects on resting metabolic rate and diet-induced thermogenesis

1990 ◽  
Vol 64 (2) ◽  
pp. 413-425 ◽  
Author(s):  
Jan A. Weststrate ◽  
Ingrid Wunnink ◽  
Paul Deurenberg ◽  
Joseph G. A. J. Hautvast
Keyword(s):  
Energy Expenditure ◽  
Metabolic Rate ◽  
Resting Metabolic Rate ◽  
Resting Energy Expenditure ◽  
Random Order ◽  
Systematic Difference ◽  
Control Treatment ◽  
Diet Induced Thermogenesis ◽  
The Impact ◽  
Thermic Effect

The impact of alcohol (ethanol) on resting energy expenditure of male non-obese volunteers was determined in two studies. In the first study the thermic effect of alcohol on resting metabolic rate (RMR) was assessed in ten male non-obese volunteers. In the second study the impact of alcohol on diet-induced thermogenesis (DIT) was determined in twelve male non-obese volunteers. Energy expenditure was measured with a ventilated-hood system. RMR was measured for 60 min with the subjects in a fasting state. In the first study subjects received in random order 20 g alcohol in concentrations of 75, 180 and 300 ml/I water respectively. After measurement of the RMR the thermic effect of alcohol was measured for 90 min. In the second study volunteers received in random order and in duplicate either a meal of food (2 MJ) plus an alcoholic aperitif (20 g alcohol in a 180 ml/1 solution) or an isoenergetic meal of food alone (2.55 MJ) plus a placebo aperitif containing no alcohol. DIT was measured for 240 min. Alcohol induced a significant thermic effect, which varied between 0.22 and 0.30 kJ/min. No systematic difference in DIT was observed among the different concentrations. DIT was not significantly affected by the ingestion of alcohol. Total DIT was 219 (SE 14) kJ for the alcohol treatment and 185 (SE 20) kJ for the control treatment. The results do not support the suggestion that alcohol is less efficiently used as an energy source in comparison with, for example, fats and carbohydrates.

Diurnal variation in postabsorptive resting metabolic rate and diet-induced thermogenesis

1989 ◽  
Vol 50 (5) ◽  
pp. 908-914 ◽  
Author(s):  
J A Weststrate ◽  
P J Weys ◽  
E J Poortvliet ◽  
P Deurenberg ◽  
J G Hautvast
Keyword(s):  
Metabolic Rate ◽  
Diurnal Variation ◽  
Resting Metabolic Rate ◽  
Diet Induced Thermogenesis
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