scholarly journals The role of RFamide peptides in feeding

2007 ◽  
Vol 192 (1) ◽  
pp. 3-15 ◽  
Author(s):  
David A Bechtold ◽  
Simon M Luckman
Keyword(s):  
Biological Activity ◽  
Energy Balance ◽  
Food Intake ◽  
Energy Expenditure ◽  
Feeding Behaviour ◽  
Animal Kingdom ◽  
Primary Function

In the three decades since FMRFamide was isolated from the clam Macrocallista nimbosa, the list of RFamide peptides has been steadily growing. These peptides occur widely across the animal kingdom, including five groups of RFamide peptides identified in mammals. Although there is tremendous diversity in structure and biological activity in the RFamides, the involvement of these peptides in the regulation of energy balance and feeding behaviour appears consistently through evolution. Even so, questions remain as to whether feeding-related actions represent a primary function of the RFamides, especially within mammals. However, as we will discuss here, the study of RFamide function is rapidly expanding and with it so is our understanding of how these peptides can influence food intake directly as well as related aspects of feeding behaviour and energy expenditure.

scholarly journals Obesity Hypertension: The Regulatory Role of Leptin

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Shilpa Kshatriya ◽  
Kan Liu ◽  
Ali Salah ◽  
Tamas Szombathy ◽  
Ronald H. Freeman ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Balance ◽  
Food Intake ◽  
Energy Expenditure ◽  
Peptide Hormone ◽  
Regulatory Role ◽  
Cardiac Damage ◽  
Obesity Hypertension ◽  
Renal Vascular

Leptin is a 16-kDa-peptide hormone that is primarily synthesized and secreted by adipose tissue. One of the major actions of this hormone is the control of energy balance by binding to receptors in the hypothalamus, leading to reduction in food intake and elevation in temperature and energy expenditure. In addition, increasing evidence suggests that leptin, through both direct and indirect mechanisms, may play an important role in cardiovascular and renal regulation. While the relevance of endogenous leptin needs further clarification, it appears to function as a pressure and volume-regulating factor under conditions of health. However, in abnormal situations characterized by chronic hyperleptinemia such as obesity, it may function pathophysiologically for the development of hypertension and possibly also for direct renal, vascular, and cardiac damage.

Role of malonyl-CoA in the hypothalamic control of food intake and energy expenditure

2005 ◽  
Vol 33 (5) ◽  
pp. 1063-1067 ◽  
Author(s):  
M.D. Lane ◽  
Z. Hu ◽  
S.-H. Cha ◽  
Y. Dai ◽  
M. Wolfgang ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Energy Balance ◽  
Food Intake ◽  
Energy Expenditure ◽  
Feeding Behaviour ◽  
Fatty Acid Synthase ◽  
Acid Synthesis ◽  
Acid Oxidation ◽  
Energy Status ◽  
Malonyl Coa

The brain plays an important role in the regulation of energy balance in higher animals. Global energy balance is monitored by sets of neurons in the hypothalamus that respond to peripheral hormonal and afferent neural signals that sense the energy status. Malonyl-CoA, an intermediate in the biosynthesis of fatty acids, appears to function in this hypothalamic energy-sensing system. The steady-state level of malonyl-CoA is determined by its rate of synthesis catalysed by ACC (acetyl-CoA carboxylase) relative to its rate of turnover catalysed by FAS (fatty acid synthase). Changes in the level of malonyl-CoA in the hypothalamus alter the expression/secretion of key hypothalamic orexigenic and anorexigenic neuropeptides that regulate the feeding behaviour and energy expenditure. Inhibitors of FAS, administered i.c.v. (intracerebroventricularly) to lean or obese mice, cause a rapid rise in hypothalamic malonyl-CoA level, suppression of food intake, increased fatty acid oxidation in skeletal muscle and profound weight loss. Stereotactic delivery of a viral MCD (malonyl-CoA decarboxylase) expression vector into the ventral hypothalamus lowers malonyl-CoA levels and reverses the anorectic effect of the FAS inhibitors. Fasting decreases, whereas refeeding increases, hypothalamic malonyl-CoA and alters subsequent feeding behaviour accordingly. The level of malonyl-CoA in the hypothalamus appears to be under the control of 5′-AMP kinase, which phosphorylates and thereby inactivates ACC under conditions of energy surplus. Thus malonyl-CoA appears to link the energy-responsive fatty acid synthesis in the hypothalamus to feeding behaviour and peripheral energy expenditure.

The role of exercise in thermogenesis and energy balance

1989 ◽  
Vol 67 (4) ◽  
pp. 402-409 ◽  
Author(s):  
Denis Richard ◽  
Serge Rivest
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Energy Expenditure ◽  
Exercise Training ◽  
Female Rats ◽  
Male Rats ◽  
Brown Adipose ◽  
Term Energy

The role of exercise training in energy balance has been reviewed. Recent well-conducted studies showed that exercise may increase energy expenditure not only during the period of exercise itself but during the postexercise period as well. This notion of excess postexercise oxygen consumption (EPOC), which has been a controversial issue for many years, is now becoming a generally well-accepted concept, the consensus being that EPOC takes place following prolonged and strenuous exercise bouts. Besides, the role of EPOC in long-term energy balance remains to be determined. Long-term energy balance studies carried out in rats show that exercise affects energy balance by altering food intake and promoting energy expenditure. In male rats exercise causes a marked decrease in energy intake which contributes, in association with the expenditure of exercise itself, to retard lean and fat tissue growth. From the suppressed deposition of lean body mass, decreases in basal metabolic rate can be predicted in males. In female rats, exercise does not affect food intake; the lower energy gain of exercise-trained females results from the elevated expenditure rate associated with exercise itself. In both male and female rats, there is no evidence that exercise training affects energy expenditure other than during exercise itself unless the habitual feeding pattern of the rats is radically modified. The interactive effects of diet and exercise, which have to be further investigated in long-term energy balance, emerge as a promising area of research.Key words: exercise training, nutritional energetics, brown adipose tissue, diet-induced thermogenesis, body composition.

scholarly journals Murine neuronatin deficiency is associated with a hypervariable food intake and bimodal obesity

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Irene Cimino ◽  
Debra Rimmington ◽  
Y. C. Loraine Tung ◽  
Katherine Lawler ◽  
Pierre Larraufie ◽  
...  
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Food Intake ◽  
Energy Expenditure ◽  
Positive Energy ◽  
Chow Diet ◽  
Chromatin Regulator ◽  
Positive Energy Balance ◽  
The Impact ◽  
Deficient Mice

AbstractNeuronatin (Nnat) has previously been reported to be part of a network of imprinted genes downstream of the chromatin regulator Trim28. Disruption of Trim28 or of members of this network, including neuronatin, results in an unusual phenotype of a bimodal body weight. To better characterise this variability, we examined the key contributors to energy balance in Nnat+/−p mice that carry a paternal null allele and do not express Nnat. Consistent with our previous studies, Nnat deficient mice on chow diet displayed a bimodal body weight phenotype with more than 30% of Nnat+/−p mice developing obesity. In response to both a 45% high fat diet and exposure to thermoneutrality (30 °C) Nnat deficient mice maintained the hypervariable body weight phenotype. Within a calorimetry system, food intake in Nnat+/−p mice was hypervariable, with some mice consuming more than twice the intake seen in wild type littermates. A hyperphagic response was also seen in Nnat+/−p mice in a second, non-home cage environment. An expected correlation between body weight and energy expenditure was seen, but corrections for the effects of positive energy balance and body weight greatly diminished the effect of neuronatin deficiency on energy expenditure. Male and female Nnat+/−p mice displayed subtle distinctions in the degree of variance body weight phenotype and food intake and further sexual dimorphism was reflected in different patterns of hypothalamic gene expression in Nnat+/−p mice. Loss of the imprinted gene Nnat is associated with a highly variable food intake, with the impact of this phenotype varying between genetically identical individuals.

scholarly journals Glycomacropeptide, a low-phenylalanine protein isolated from cheese whey, supports growth and attenuates metabolic stress in the murine model of phenylketonuria

2012 ◽  
Vol 302 (7) ◽  
pp. E885-E895 ◽  
Author(s):  
Patrick Solverson ◽  
Sangita G. Murali ◽  
Adam S. Brinkman ◽  
David W. Nelson ◽  
Murray K. Clayton ◽  
...  
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Energy Expenditure ◽  
Lean Mass ◽  
Metabolic Stress ◽  
Casein Diet ◽  
Wild Type ◽  
Total Fat ◽  
Spleen Mass ◽  
Main Effects

Phenylketonuria (PKU) is caused by a mutation in the phenylalanine (phe) hydroxylase gene and requires a low-phe diet plus amino acid (AA) formula to prevent cognitive impairment. Glycomacropeptide (GMP) contains minimal phe and provides a palatable alternative to AA formula. Our objective was to compare growth, body composition, and energy balance in Pahenu2 (PKU) and wild-type mice fed low-phe GMP, low-phe AA, or high-phe casein diets from 3–23 wk of age. The 2 × 2 × 3 design included main effects of genotype, sex, and diet. Fat and lean mass were assessed by dual-energy X-ray absorptiometry, and acute energy balance was assessed by indirect calorimetry. PKU mice showed growth and lean mass similar to wild-type littermates fed the GMP or AA diets; however, they exhibited a 3–15% increase in energy expenditure, as reflected in oxygen consumption, and a 3–30% increase in food intake. The GMP diet significantly reduced energy expenditure, food intake, and plasma phe concentration in PKU mice compared with the casein diet. The high-phe casein diet or the low-phe AA diet induced metabolic stress in PKU mice, as reflected in increased energy expenditure and intake of food and water, increased renal and spleen mass, and elevated plasma cytokine concentrations consistent with systemic inflammation. The low-phe GMP diet significantly attenuated these adverse effects. Moreover, total fat mass, %body fat, and the respiratory exchange ratio (CO2 produced/O2 consumed) were significantly lower in PKU mice fed GMP compared with AA diets. In summary, GMP provides a physiological source of low-phe dietary protein that promotes growth and attenuates the metabolic stress induced by a high-phe casein or low-phe AA diet in PKU mice.

Energy balance and food intake: The role of PPARγ gene polymorphisms

2006 ◽  
Vol 88 (3) ◽  
pp. 227-233 ◽  
Author(s):  
Joanne E. Cecil ◽  
Peter Watt ◽  
Colin N. Palmer ◽  
Marion Hetherington
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Gene Polymorphisms ◽  
Pparγ Gene

Use of doubly labeled water technique in soldiers training for jungle warfare

1989 ◽  
Vol 67 (1) ◽  
pp. 14-18 ◽  
Author(s):  
C. H. Forbes-Ewan ◽  
B. L. Morrissey ◽  
G. C. Gregg ◽  
D. R. Waters
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Energy Expenditure ◽  
Daily Intake ◽  
Doubly Labeled Water ◽  
Daily Energy Expenditure ◽  
Balance Study ◽  
Wide Range ◽  
Daily Energy ◽  
Doubly Labeled Water Method

The doubly labeled water method was used to estimate the energy expended by four members of an Australian Army platoon (34 soldiers) engaged in training for jungle warfare. Each subject received an oral isotope dose sufficient to raise isotope levels by 200–250 (18O) and 100–120 ppm (2H). The experimental period was 7 days. Concurrently, a factorial estimate of the energy expenditure of the platoon was conducted. Also, a food intake-energy balance study was conducted for the platoon. Mean daily energy expenditure by the doubly labeled water method was 4,750 kcal (range 4,152–5,394 kcal). The factorial estimate of mean daily energy expenditure was 4,535 kcal. Because of inherent inaccuracies in the food intake-energy balance technique, we were able to conclude only that energy expenditure, as measured by this method, was greater than the estimated mean daily intake of 4,040 kcal. The doubly labeled water technique was well tolerated, is noninvasive, and appears to be suitable in a wide range of field applications.

Coinjection of CCK and leptin reduces food intake via increased CART/TRH and reduced AMPK phosphorylation in the hypothalamus

2014 ◽  
Vol 306 (11) ◽  
pp. E1284-E1291 ◽  
Author(s):  
Sayaka Akieda-Asai ◽  
Paul-Emile Poleni ◽  
Yukari Date
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Interactive Effect ◽  
Reduce Food Intake ◽  
Mrna Levels ◽  
Neural Pathway ◽  
Ampk Phosphorylation ◽  
Amp Activated Protein Kinase ◽  
Insight Into

CCK and leptin are anorectic hormones produced in the small intestine and white adipose tissue, respectively. Investigating how these hormones act together as an integrated anorectic signal is important for elucidating the mechanisms by which energy balance is maintained. We found here that coadministration of subthreshold CCK and leptin, which individually have no effect on feeding, dramatically reduced food intake in rats. Phosphorylation of AMP-activated protein kinase (AMPK) in the hypothalamus significantly decreased after coinjection of CCK and leptin. In addition, coadministration of these hormones significantly increased mRNA levels of anorectic cocaine- and amphetamine-regulated transcript (CART) and thyrotropin-releasing hormone (TRH) in the hypothalamus. The interactive effect of CCK and leptin on food intake was abolished by intracerebroventricular preadministration of the AMPK activator AICAR or anti-CART/anti-TRH antibodies. These findings indicate that coinjection of CCK and leptin reduces food intake via reduced AMPK phosphorylation and increased CART/TRH in the hypothalamus. Furthermore, by using midbrain-transected rats, we investigated the role of the neural pathway from the hindbrain to the hypothalamus in the interaction of CCK and leptin to reduce food intake. Food intake reduction induced by coinjection of CCK and leptin was blocked in midbrain-transected rats. Therefore, the neural pathway from hindbrain to hypothalamus plays an important role in transmitting the anorectic signals provided by coinjection of CCK and leptin. Our findings give further insight into the mechanisms of feeding and energy balance.

scholarly journals Long-term effects of ghrelin and ghrelin receptor agonists on energy balance in rats

2008 ◽  
Vol 295 (1) ◽  
pp. E78-E84 ◽  
Author(s):  
Sabine Strassburg ◽  
Stefan D. Anker ◽  
Tamara R. Castaneda ◽  
Lukas Burget ◽  
Diego Perez-Tilve ◽  
...  
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Food Intake ◽  
Energy Expenditure ◽  
Therapeutic Potential ◽  
Body Weight Gain ◽  
Metabolic Effects ◽  
Positive Energy ◽  
High Dose ◽  
Growth Hormone Secretagogue

Ghrelin, an endogenous ligand of the growth hormone secretagogue receptor (GHS-R), is the only circulating agent to powerfully promote a positive energy balance. Such action is mediated predominantly by central nervous system pathways controlling food intake, energy expenditure, and nutrient partitioning. The ghrelin pathway may therefore offer therapeutic potential for the treatment of catabolic states. However, the potency of the endogenous hormone ghrelin is limited due to a short half-life and the fragility of its bioactivity ensuring acylation at serine 3. Therefore, we tested the metabolic effects of two recently generated GHS-R agonists, BIM-28125 and BIM-28131, compared with ghrelin. All agents were administered continuously for 1 mo in doses of 50 and 500 nmol·kg−1·day−1 using implanted subcutaneous minipumps in rats. High-dose treatment with single agonists or ghrelin increased body weight gain by promoting fat mass, whereas BIM-28131 was the only one also increasing lean mass significantly. Food intake increased during treatment with BIM-28131 or ghrelin, whereas no effects on energy expenditure were detected. With the lower dose, only BIM-28131 had a significant effect on body weight. This also held true when the compound was administered by subcutaneous injection three times/day. No symptoms or signs of undesired effects were observed in any of the studies or treated groups. These results characterize BIM-28131 as a promising GHS-R agonist with an attractive action profile for the treatment of catabolic disease states such as cachexia.

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