scholarly journals Does body mass play a role in the regulation of food intake?

2002 ◽  
Vol 61 (4) ◽  
pp. 473-487 ◽  
Author(s):  
John R. Speakman ◽  
R. James Stubbs ◽  
Julian G. Mercer
Keyword(s):  
Food Intake ◽  
Energy Expenditure ◽  
Body Mass ◽  
Body Fat ◽  
Body Fatness ◽  
Total Body Mass ◽  
Energy Imbalance ◽  
Fat Stores ◽  
The Brain ◽  
Different Levels

It is widely believed that body fatness (and hence total body mass) is regulated by a lipostatic feedback system. This system is suggested to involve at least one peripheral signalling compound, which signals to the brain the current size of body fat stores. In the brain the level of the signal is compared with a desirable target level, and food intake and energy expenditure are then regulated to effect changes in the size of body fat stores. There is considerable support for this theory at several different levels of investigation. Patterns of body-mass change in subjects forced into energy imbalance seem to demonstrate homeostasis, and long-term changes in body mass are minor compared with the potential changes that might result from energy imbalance. Molecular studies of signalling compounds have suggested a putative lipostatic signal (leptin) and a complex network of downstream processing events in the brain, polymorphisms of which lead to disruption of body-mass regulation. This network of neuropeptides provides a rich seam of potential pharmaceutical targets for the control of obesity. Despite this consistent explanation for the observed phenomena at several different levels of enquiry, there are alternative explanations. In the present paper we explore the possibility that the existence of lipostatic regulation of body fatness is an illusion generated by the links between body mass and energy expenditure and responses to energy imbalance that are independent of body mass. Using computer-based models of temporal patterns in energy balance we show that common patterns of change in body mass following perturbation can be adequately explained by this ‘non-lipostatic’ model. This model has some important implications for the interpretations that we place on the molecular events in the brain, and ultimately in the search for pharmaceutical agents for alleviation of obesity.

scholarly journals Increased energy expenditure and leptin sensitivity account for low fat mass in myostatin-deficient mice

2011 ◽  
Vol 300 (6) ◽  
pp. E1031-E1037 ◽  
Author(s):  
Sun Ju Choi ◽  
Zipora Yablonka-Reuveni ◽  
Karl J. Kaiyala ◽  
Kayoko Ogimoto ◽  
Michael W. Schwartz ◽  
...  
Keyword(s):  
Food Intake ◽  
Energy Expenditure ◽  
Body Mass ◽  
Body Fat ◽  
Fat Mass ◽  
Body Fat Mass ◽  
Low Fat ◽  
Total Body Mass ◽  
Leptin Sensitivity ◽  
Deficient Mice

Myostatin deficiency causes dramatically increased skeletal muscle mass and reduced fat mass. Previously, myostatin-deficient mice were reported to have unexpectedly low total energy expenditure (EE) after normalizing to body mass, and thus, a metabolic cause for low fat mass was discounted. To clarify how myostatin deficiency affects the control of body fat mass and energy balance, we compared rates of oxygen consumption, body composition, and food intake in young myostatin-deficient mice relative to wild-type (WT) and heterozygous (HET) controls. We report that after adjusting for total body mass using regression analysis, young myostatin-deficient mice display significantly increased EE relative to both WT (+0.81 ± 0.28 kcal/day, P = 0.004) and HET controls (+0.92 ± 0.31 kcal/day, P = 0.005). Since food intake was not different between groups, increased EE likely accounts for the reduced body fat mass (KO: 8.8 ± 1.1% vs. WT: 14.5 ± 1.3%, P = 0.003) and circulating leptin levels (KO: 0.7 ± 0.2 ng/ml vs. WT: 1.9 ± 0.3 ng/ml, P = 0.008). Interestingly, the observed increase in adjusted EE in myostatin-deficient mice occurred despite dramatically reduced ambulatory activity levels (−50% vs. WT, P < 0.05). The absence of hyperphagia together with increased EE in myostatin-deficient mice suggests that increased leptin sensitivity may contribute to their lean phenotype. Indeed, leptin-induced anorexia (KO: −17 ± 1.2% vs. WT: −5 ± 0.3%) and weight loss (KO: −2.2 ± 0.2 g vs. WT: −1.6 ± 0.1, P < 0.05) were increased in myostatin-deficient mice compared with WT controls. We conclude that increased EE, together with increased leptin sensitivity, contributes to low fat mass in mice lacking myostatin.

Serum leptin levels and energy expenditure in normal weight women

1998 ◽  
Vol 76 (2) ◽  
pp. 237-241 ◽  
Author(s):  
L J Martin ◽  
PJH Jones ◽  
R V Considine ◽  
W Su ◽  
N F Boyd ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Food Intake ◽  
Energy Expenditure ◽  
Body Mass ◽  
Body Fat ◽  
Positive Association ◽  
Normal Weight ◽  
Serum Leptin ◽  
Percentage Body Fat ◽  
Healthy Humans

To investigate whether circulating leptin levels are associated with energy expenditure in healthy humans, doubly labeled water energy measurements and food intake assessment were carried out in 27 women (mean age, 48.6 years; weight, 61.9 kg; body mass index, 23.2). Energy expenditure was determined over 13 days. Food intake was measured by 7-day food records. Leptin was measured by radioimmunoassay. Leptin level was strongly associated with percentage body fat (r = 0.59; p < 0.001), fat mass (r = 0.60; p < 0.001), and body mass index (r = 0.41; p = 0.03), but no correlation was observed with energy expenditure (r = 0.02; p = 0.93). After controlling for percentage body fat, a positive association of leptin level with energy expenditure of marginal significance (p = 0.06) was observed. There were no significant univariate associations of age, physical activity, lean body mass, height, or dietary variables with leptin level. When controlling for body fat, a significant positive correlation was observed for percent energy from carbohydrate and negative correlations with dietary fat and alcohol intake. These findings confirm previous associations between leptin and body fat content and suggest a relationship between serum leptin and energy expenditure level in healthy humans.Key words: leptin, energy expenditure, body composition, diet.

Plasma leptin in transition dairy cows. Effects of body fatness, ambient temperature and dietary factors

2002 ◽  
Vol 2002 ◽  
pp. 92-92 ◽  
Author(s):  
T. Kokkonen ◽  
J. Taponen ◽  
S. Alasuutari ◽  
M. Nousiainen ◽  
T. Anttila ◽  
...  
Keyword(s):  
Food Intake ◽  
Energy Expenditure ◽  
Dairy Cows ◽  
Dairy Cow ◽  
Dietary Factors ◽  
Body Fatness ◽  
Increase Energy Expenditure ◽  
Transition Dairy Cows ◽  
Cow Performance ◽  
Plasma Leptin

In ruminants plasma leptin is increased with increasing body fatness. Leptin acts on hypothalamus to decrease food intake and increase energy expenditure. It is possible that leptin has a key role in transition from pregnancy to lactation of dairy cows. The objective of the present work was to investigate the pattern of plasma leptin concentration, as well as its relationship with other hormones and metabolites and dairy cow performance.

scholarly journals Whole-Food Plant-Based Lifestyle Program and Decreased Obesity: A 10-Year Follow-up

2019 ◽  
Author(s):  
Boštjan Jakše ◽  
Barbara Jakše ◽  
Stanislav Pinter ◽  
Jernej Pajek ◽  
Nataša Fidler Mis
Keyword(s):  
Body Composition ◽  
Body Mass ◽  
Body Fat ◽  
Food Plant ◽  
Body Fat Percentage ◽  
Fat Percentage ◽  
Total Body Mass ◽  
Lifestyle Program ◽  
Composition Changes

Failure of various weight-loss programs and long-term maintenance of favorable body composition in all kinds of people is high, since the majority go back to old dietary patterns. Many studies have documented the efficacy of a plant-based diet (PBD) for body mass management, but there are opinions that maintaining a PBD is difficult. We aimed to evaluate the long-term success of a whole-food plant-based (WFPB) lifestyle program. We investigated the differences in the obesity indices and lifestyle of 151 adults (39.6 &plusmn; SD 12.5 years), who were on our program for short (0.5&ndash;&lt;2 years), medium (2&ndash;&lt;5 years), or long term (5&ndash;10 years). Body-composition changes were favourable for all three groups, both genders and all participants. There were no differences in relative body-composition changes (BMI, body fat percentage and muscle mass index (MMI)) between the three groups. All participants improved their BMI (baseline mean pre-obesity BMI range (kg/m2): 26.4 &plusmn; 5.6 to normal 23.9 &plusmn; 3.8, p &lt; 0.001), decreased body mass (&ndash;7.1 &plusmn; 8.3 kg, p &lt; 0.001) and body fat percentage (&ndash;6.4 &plusmn; 5.6 % points, p &lt; 0.001). 85.6% (101 out of 118) of parents of underage children (&lt; 18 years), introduced WFPB lifestyle to their children. Those with the highest BMI at baseline lost the most of: a) BMI units, b) total body mass and c) body fat (a) (kg/m2) (&ndash;5.6 &plusmn; SD 2.9, &ndash;2.4 &plusmn; 1.8 and &ndash;0.9 &plusmn; 1.5), b) (kg) (&ndash;16.1 &plusmn; SD 8.8, &ndash;7.1 &plusmn; 5.4 and &ndash;2.5 &plusmn; 4.5) and c) (% points) (&ndash;9.5 &plusmn; SD 5.7, &ndash;6.6 &plusmn; 4.6 and &ndash;4.7 &plusmn; 5.3) for participants who had baseline BMI in obese, overweight and normal range, respectively; pbaseline vs. current &lt; 0.001 for all). WFPB lifestyle program provides long-term lifestyle changes for reversal of obesity and is effective transferred to the next generation.

scholarly journals Effects of Chronic Intracerebroventricular Infusion of RFamide-Related Peptide-3 on Energy Metabolism in Male Mice

2020 ◽  
Vol 21 (22) ◽  
pp. 8606
Author(s):  
Shogo Moriwaki ◽  
Yuki Narimatsu ◽  
Keisuke Fukumura ◽  
Eiko Iwakoshi-Ukena ◽  
Megumi Furumitsu ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Metabolism ◽  
Food Intake ◽  
Energy Expenditure ◽  
Body Mass ◽  
The Other ◽  
Related Peptide ◽  
Intracerebroventricular Infusion ◽  
Brown Adipose ◽  
The Masses

RFamide-related peptide-3 (RFRP-3), the mammalian ortholog of avian gonadotropin-inhibitory hormone (GnIH), plays a crucial role in reproduction. In the present study, we explored the other functions of RFRP-3 by investigating the effects of chronic intracerebroventricular infusion of RFRP-3 (6 nmol/day) for 13 days on energy homeostasis in lean male C57BL/6J mice. The infusion of RFRP-3 increased cumulative food intake and body mass. In addition, the masses of brown adipose tissue (BAT) and the liver were increased by the administration of RFRP-3, although the mass of white adipose tissue was unchanged. On the other hand, RFRP-3 decreased O2 consumption, CO2 production, energy expenditure, and core body temperature during a short time period in the dark phase. These results suggest that the increase in food intake and the decrease in energy expenditure contributed to the gain of body mass, including the masses of BAT and the liver. The present study shows that RFRP-3 regulates not only reproductive function, but also energy metabolism, in mice.

scholarly journals Endocrine factors in the hypothalamic regulation of food intake in females: a review of the physiological roles and interactions of ghrelin, leptin, thyroid hormones, oestrogen and insulin

2011 ◽  
Vol 24 (1) ◽  
pp. 132-154 ◽  
Author(s):  
V. Somogyi ◽  
A. Gyorffy ◽  
T. J. Scalise ◽  
D. S. Kiss ◽  
G. Goszleth ◽  
...  
Keyword(s):  
Food Intake ◽  
Energy Expenditure ◽  
Thyroid Hormones ◽  
Energy Homeostasis ◽  
The Body ◽  
Feedback Information ◽  
Hypothalamic Regulation ◽  
The Individual ◽  
Desire To Eat ◽  
The Brain

Controlling energy homeostasis involves modulating the desire to eat and regulating energy expenditure. The controlling machinery includes a complex interplay of hormones secreted at various peripheral endocrine endpoints, such as the gastrointestinal tract, the adipose tissue, thyroid gland and thyroid hormone-exporting organs, the ovary and the pancreas, and, last but not least, the brain itself. The peripheral hormones that are the focus of the present review (ghrelin, leptin, thyroid hormones, oestrogen and insulin) play integrated regulatory roles in and provide feedback information on the nutritional and energetic status of the body. As peripheral signals, these hormones modulate central pathways in the brain, including the hypothalamus, to influence food intake, energy expenditure and to maintain energy homeostasis. Since the growth of the literature on the role of various hormones in the regulation of energy homeostasis shows a remarkable and dynamic expansion, it is now becoming increasingly difficult to understand the individual and interactive roles of hormonal mechanisms in their true complexity. Therefore, our goal is to review, in the context of general physiology, the roles of the five best-known peripheral trophic hormones (ghrelin, leptin, thyroid hormones, oestrogen and insulin, respectively) and discuss their interactions in the hypothalamic regulation of food intake.

Predicting the effects of body fatness on food intake and performance of sheep

2005 ◽  
Vol 2005 ◽  
pp. 16-16
Author(s):  
B. J. Tolkamp ◽  
J. M. Yearsley ◽  
I. Kyriazakis
Keyword(s):  
Food Intake ◽  
Energy Expenditure ◽  
Live Weight ◽  
Body Lipid ◽  
Body Fatness ◽  
Ewe Lambs ◽  
Test Models ◽  
Condition Score ◽  
And Performance ◽  
Using Data

Food intake (FI) can be predicted on the basis of variables that describe food quality and the animal. Live weight (LW) is usually the only variable that is used to describe the animal. Animal fatness, as estimated by condition score (CS), can affect FI at a given LW. Body lipid produces signals (leptin) that affect energy intake and energy expenditure. If fatness acts on intake via its effect on energy expenditure, the effects of body lipid content on food intake can be incorporated into an existing intake model. Our objectives were to construct and test models that predict effects of fatness on intake and performance, using data obtained with ewe lambs to parameterise and test the models.

A note on the effects of body fatness and level of food intake on the rate of fat loss in lactating ewes

1982 ◽  
Vol 34 (3) ◽  
pp. 355-357 ◽  
Author(s):  
R. T. Cowan ◽  
J. J. Robinson ◽  
I. McDonald
Keyword(s):  
Food Intake ◽  
Energy Intake ◽  
Body Fat ◽  
Metabolizable Energy ◽  
Body Fatness ◽  
Fat Loss ◽  
Body Fat Content ◽  
Metabolizable Energy Intake ◽  
Image Position ◽  
The Relationship

ABSTRACTData from three comparative slaughter experiments involving a total of 73 ewes were used to study the influence of body fat content at the start of lactation (X1 kg) and of metabolizable energy intake (X2, MJ/day), on the rate of loss of body fat by lactating ewes over the first 6 weeks of lactation (Y, g/day). The relationship was described by the equation:Thus the rate of fat loss was greater for ewes with higher initial fat contents, but the differential became less as metabolizable energy intake increased. Since increases in body fatness depress food intake it was not possible to prevent loss of body fat during early lactation in fat ewes given high concentrate diets ad libitum. The likely response in milk yield to increase in body fatness at parturition is therefore strongly dependent on the relative levels of body fatness and metabolizable energy intake. The value of any improvement in condition of the ewe at parturition may be considerable when metabolizable energy intake during lactation is low but much less when it is expected to be high.

scholarly journals The effects of physiological adaptations to calorie restriction on global cell proliferation rates

2011 ◽  
Vol 300 (4) ◽  
pp. E735-E745 ◽  
Author(s):  
Matthew D. Bruss ◽  
Airlia C. S. Thompson ◽  
Ishita Aggarwal ◽  
Cyrus F. Khambatta ◽  
Marc K. Hellerstein
Keyword(s):  
Cell Proliferation ◽  
Body Weight ◽  
Food Intake ◽  
Energy Expenditure ◽  
Body Fat ◽  
Calorie Restriction ◽  
Percent Body Fat ◽  
Female Mice ◽  
Physiological Adaptations ◽  
Running Wheels

Calorie restriction (CR) reduces the rate of cell proliferation in mitotic tissues. It has been suggested that this reduction in cell proliferation may mediate CR-induced increases in longevity. However, the mechanisms that lead to CR-induced reductions in cell proliferation rates remain unclear. To evaluate the CR-induced physiological adaptations that may mediate reductions in cell proliferation rates, we altered housing temperature and access to voluntary running wheels to determine the effects of food intake, energy expenditure, percent body fat, and body weight on proliferation rates of keratinocytes, liver cells, mammary epithelial cells, and splenic T-cells in C57BL/6 mice. We found that ∼20% CR led to a reduction in cell proliferation rates in all cell types. However, lower cell proliferation rates were not observed with reductions in 1) food intake and energy expenditure in female mice housed at 27°C, 2) percent body fat in female mice provided running wheels, or 3) body weight in male mice provided running wheels compared with ad libitum-fed controls. In contrast, reductions in insulin-like growth factor I were associated with decreased cell proliferation rates. Taken together, these data suggest that CR-induced reductions in food intake, energy expenditure, percent body fat, and body weight do not account for the reductions in global cell proliferation rates observed in CR. In addition, these data are consistent with the hypothesis that reduced cell proliferation rates could be useful as a biomarker of interventions that increase longevity.

scholarly journals Inconsistencies in the assessment of food intake

2012 ◽  
Vol 303 (12) ◽  
pp. E1408-E1418 ◽  
Author(s):  
Stephen C. Woods ◽  
Wolfgang Langhans
Keyword(s):  
Food Intake ◽  
Energy Intake ◽  
Body Fat ◽  
Energy Homeostasis ◽  
Behavioral Responses ◽  
Normal Function ◽  
Direct Proportion ◽  
Heated Debate ◽  
The Brain ◽  
Reducing Energy

Many peptides and other compounds that influence metabolism also influence food intake, and numerous hypotheses explaining the observed effects in terms of energy homeostasis have been suggested over the years. For example, cholecystokinin (CCK), a duodenal peptide secreted during meals that aids in digestion, also reduces ongoing food intake, thereby contributing to satiation; and insulin and leptin, hormones secreted in direct proportion to body fat, act in the brain to help control adiposity by reducing energy intake. These behavioral actions are often considered to be hard-wired, such that negative experiments, in which an administered compound fails to have its purported effect, are generally disregarded. In point of fact, failures to replicate the effects of compounds on food intake are commonplace, and this occurs both between and within laboratories. Failures to replicate have historically fueled heated debate about the efficacy and/or normal function of one or another compound, leading to confusion and ambiguity in the literature. We review these phenomena and their implications and argue that, rather than eliciting hard-wired behavioral responses in the maintenance of homeostasis, compounds that alter food intake are subjected to numerous influences that can render them completely ineffective at times and that a major reason for this variance is that food intake is not under stringent homeostatic control.

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