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

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 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.

Hypophagic effects of insulin are mediated via NPY1/NPY2 receptors in broiler cockerels

2018 ◽  
Vol 96 (12) ◽  
pp. 1301-1307 ◽  
Author(s):  
Shiba Yousefvand ◽  
Farshid Hamidi ◽  
Morteza Zendehdel ◽  
Abbas Parham
Keyword(s):  
Blood Glucose ◽  
Energy Balance ◽  
Food Intake ◽  
Control Group ◽  
Control Solution ◽  
Treatment Groups ◽  
Insulin Control ◽  
And Control ◽  
Npy Receptors

Neuropeptide Y (NPY) plays a mediatory role in cerebral insulin function by maintaining energy balance. The current study was designed to determine the role of insulin in food intake and its interaction with NPY receptors in 8 experiments using broiler cockerels (4 treatment groups per experiment, except for experiment 8). Chicks received control solution or 2.5, 5, or 10 ng of insulin in experiment 1 and control solution or 1.25, 2.5, or 5 μg of receptor antagonists B5063, SF22, or SML0891 in experiments 2, 3, and 4 through intracerebroventricular (ICV) injection, respectively. In experiments 5, 6, and 7, chicks received ICV injection of B5063, SF22, SML0891, or co-injection of an antagonist + insulin, control solution, and insulin. In experiment 8, blood glucose was measured. Insulin, B5063, and SML0891 decreased food intake, while SF22 led to an increase in food intake. The hypophagic effect of insulin was also reinforced by injection of B560, but ICV injection of SF22 destroyed this hypophagic effect of insulin and increased food intake (p < 0.05). However, SML0891 had no effect on decreased food intake induced by insulin (p > 0.05). At 30 min postinjection, blood sugar in the control group was higher than that in the insulin group (p < 0.05). Therefore, the NPY1 and NPY2 receptors mediate the hypophagic effect of insulin in broiler cockerels.

scholarly journals Glial Modulation of Energy Balance: The Dorsal Vagal Complex Is No Exception

2022 ◽  
Vol 23 (2) ◽  
pp. 960
Author(s):  
Jean-Denis Troadec ◽  
Stéphanie Gaigé ◽  
Manon Barbot ◽  
Bruno Lebrun ◽  
Rym Barbouche ◽  
...  
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Glial Cells ◽  
Present Review ◽  
Dorsal Vagal Complex ◽  
Central Regulation ◽  
The World ◽  
Nutritional Imbalance ◽  
Nutritional Balance

The avoidance of being overweight or obese is a daily challenge for a growing number of people. The growing proportion of people suffering from a nutritional imbalance in many parts of the world exemplifies this challenge and emphasizes the need for a better understanding of the mechanisms that regulate nutritional balance. Until recently, research on the central regulation of food intake primarily focused on neuronal signaling, with little attention paid to the role of glial cells. Over the last few decades, our understanding of glial cells has changed dramatically. These cells are increasingly regarded as important neuronal partners, contributing not just to cerebral homeostasis, but also to cerebral signaling. Our understanding of the central regulation of energy balance is part of this (r)evolution. Evidence is accumulating that glial cells play a dynamic role in the modulation of energy balance. In the present review, we summarize recent data indicating that the multifaceted glial compartment of the brainstem dorsal vagal complex (DVC) should be considered in research aimed at identifying feeding-related processes operating at this level.

Eat, run, and…shiver? From the exercise – diet and energy balance symposium at CSEP 2005

2007 ◽  
Vol 32 (3) ◽  
pp. 503-504
Author(s):  
Éric Doucet
Keyword(s):  
Weight Loss ◽  
Energy Balance ◽  
Food Intake ◽  
Exercise Physiology ◽  
Canadian Society ◽  
Short Introduction ◽  
Novel Proteins ◽  
Treatment Of Obesity ◽  
Successful Weight Loss

This short introduction includes a brief description of papers that were prepared following the “Symposium on Exercise – Diet and Energy Balance”, which was presented at the Canadian Society for Exercise Physiology annual meeting in the autumn of 2005. Briefly, these three papers discuss findings related to (i) the emerging role of exercise in the treatment of obesity and its co-morbidities, (ii) the role of novel proteins secreted by fat, and (iii) the control of appetite and food intake after successful weight loss.

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.

scholarly journals Role of Dorsomedial Hypothalamic Neuropeptide Y in Modulating Food Intake and Energy Balance

2009 ◽  
Vol 29 (1) ◽  
pp. 179-190 ◽  
Author(s):  
L. Yang ◽  
K. A. Scott ◽  
J. Hyun ◽  
K. L. Tamashiro ◽  
N. Tray ◽  
...  
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Neuropeptide Y

scholarly journals Regulation of Food Intake and Gonadotropin-Releasing Hormone/Luteinizing Hormone during Lactation: Role of Insulin and Leptin

Endocrinology ◽  
2009 ◽  
Vol 150 (9) ◽  
pp. 4231-4240 ◽  
Author(s):  
Jing Xu ◽  
Melissa A. Kirigiti ◽  
Kevin L. Grove ◽  
M. Susan Smith
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Negative Energy ◽  
Serum Glucose ◽  
Negative Energy Balance ◽  
Serum Lh ◽  
Low Levels ◽  
Agouti Related Protein ◽  
Insulin Replacement

Abstract Negative energy balance during lactation is reflected by low levels of insulin and leptin and is associated with chronic hyperphagia and suppressed GnRH/LH activity. We studied whether restoration of insulin and/or leptin to physiological levels would reverse the lactation-associated hyperphagia, changes in hypothalamic neuropeptide expression [increased neuropeptide Y (NPY) and agouti-related protein (AGRP) and decreased proopiomelanocortin (POMC), kisspeptin (Kiss1), and neurokinin B (NKB)] and suppression of LH. Ovariectomized lactating rats (eight pups) were treated for 48 h with sc minipumps containing saline, human insulin, or rat leptin. The arcuate nucleus (ARH) was analyzed for NPY, AGRP, POMC, Kiss1, and NKB mRNA expression; the dorsal medial hypothalamus (DMH) was analyzed for NPY mRNA. Insulin replacement reversed the increase in ARH NPY/AGRP mRNAs, partially recovered POMC, but had no effect on recovering Kiss1/NKB. Leptin replacement only affected POMC, which was fully recovered. Insulin/leptin dual replacement had similar effects as insulin replacement alone but with a slight increase in Kiss1/NKB. The lactation-induced increase in DMH NPY was unchanged after treatments. Restoration of insulin and/or leptin had no effect on food intake, body weight, serum glucose or serum LH. These results suggest that the negative energy balance of lactation is not required for the hyperphagic drive, although it is involved in the orexigenic changes in the ARH. The chronic hyperphagia of lactation is most likely sustained by the induction of NPY in the DMH. The negative energy balance also does not appear to be a necessary prerequisite for the suppression of GnRH/LH activity.

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