Energy homeostasis imbalance in relation to depressive disorders in patients of early reproductive age with excessive body weight

2020 ◽  
Vol 16 (1) ◽  
pp. 101-115
Author(s):  
E.P Khashchenko ◽  
◽  
E.V. Uvarova ◽  
M.Yu. Vysokikh ◽  
I.A. Salnikova ◽  
...  
Keyword(s):  
Body Weight ◽  
Energy Homeostasis ◽  
Depressive Disorders ◽  
Reproductive Age ◽  
Excessive Body Weight

Behavioural Biology and Obesity

2012 ◽  
Author(s):  
Trenton G. Smith
Keyword(s):  
Body Weight ◽  
Energy Homeostasis ◽  
Population Level ◽  
Broad Array ◽  
Excessive Body Weight ◽  
Calorie Diet ◽  
Behavioural Biology ◽  
The Impact ◽  
Starvation Risk ◽  
High Calorie Diet

While conventional wisdom holds that excessive body weight is the product of some combination of a high-calorie diet and a sedentary lifestyle, public health measures aimed at these factors have been met with only limited success. This chapter considers the possibility that obesity might be better understood in terms of the biologist's notion that humans and other animals evolved the ability to store body fat as an optimal response to the presence of starvation risk. Evidence from a broad array of disciplines is consistent with this view, including the neuroendocrinology of energy homeostasis, parallels between human and animal fattening behaviour, the effect of stress on dietary intake, population-level studies of the impact of economic insecurity on body weight and international variation in obesity rates.

scholarly journals Effect of Excessive Body Weight and Emotional Disorders on the Course of Pregnancy and Well-Being of a Newborn before and during COVID-19 Pandemic

2021 ◽  
Vol 10 (4) ◽  
pp. 656
Author(s):  
Artur Wdowiak ◽  
Marta Makara-Studzińska ◽  
Dorota Raczkiewicz ◽  
Paula Janczyk ◽  
Aneta Słabuszewska-Jóźwiak ◽  
...  
Keyword(s):  
Body Weight ◽  
Emotional Disorders ◽  
Depressive Disorders ◽  
Well Being ◽  
Class Ii ◽  
Normal Weight ◽  
Obese Women ◽  
Excessive Body Weight ◽  
Negative Effect ◽  
Severity Of Depression

This study aimed to evaluate whether excessive body weight and the COVID-19 pandemic affect depression, and subsequently whether depression, excessive body weight, and the COVID-19 pandemic affect the course of pregnancy, as well as the well-being of a newborn. The research material included data retrieved from the medical records of 280 pregnant women who were provided with care by medical facilities in Lublin (100 women with normal weight, 100 overweight women, 50 with Class I and 30 with Class II obesity). They completed a Beck depression inventory (BDI) in pregnancy twice, in order to assess the risk of occurrence of postpartum depression. Pre-pregnancy BMI positively correlated with the severity of depression, both at 10–13 weeks of pregnancy (p < 0.001), and at 32 weeks of pregnancy (p < 0.001). The higher the pre-pregnancy BMI, on average the higher the severity of depression. The severity of depression was significantly higher during the pandemic than before it in women with normal body weight before pregnancy (p < 0.001), as well as in those overweight (p < 0.001) and with Class II obesity (p = 0.015). Excessive body weight before pregnancy leads to depressive disorders during pregnancy, increases the risk of preterm delivery, and exerts a negative effect on the state of a newborn. Depressive symptoms among pregnant, overweight and obese women intensified during the COVID-19 pandemic.

Central Histamine, the H3-Receptor and Obesity Therapy

2019 ◽  
Vol 18 (7) ◽  
pp. 516-522
Author(s):  
Néstor F. Díaz ◽  
Héctor Flores-Herrera ◽  
Guadalupe García-López ◽  
Anayansi Molina-Hernández
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Animal Studies ◽  
Energy Homeostasis ◽  
Receptor Activation ◽  
Receptor Ligands ◽  
Histaminergic System ◽  
H3 Receptor ◽  
Weight One ◽  
The Central Nervous System

The brain histaminergic system plays a pivotal role in energy homeostasis, through H1- receptor activation, it increases the hypothalamic release of histamine that decreases food intake and reduces body weight. One way to increase the release of hypothalamic histamine is through the use of antagonist/inverse agonist for the H3-receptor. Histamine H3-receptors are auto-receptors and heteroreceptors located on the presynaptic membranes and cell soma of neurons, where they negatively regulate the synthesis and release of histamine and other neurotransmitters in the central nervous system. Although several compounds acting as H3-receptor antagonist/inverse agonists have been developed, conflicting results have been reported and only one has been tested as anti-obesity in humans. Animal studies revealed the opposite effect in food intake, energy expeditor, and body weight, depending on the drug, spice, and route of administration, among others. The present review will explore the state of art on the effects of H3-receptor ligands on appetite and body-weight, going through the following: a brief overview of the circuit involved in the control of food intake and energy homeostasis, the participation of the histaminergic system in food intake and body weight, and the H3-receptor as a potential therapeutic target for obesity.

scholarly journals Neither Agouti-Related Protein nor Neuropeptide Y Is Critically Required for the Regulation of Energy Homeostasis in Mice

2002 ◽  
Vol 22 (14) ◽  
pp. 5027-5035 ◽  
Author(s):  
Su Qian ◽  
Howard Chen ◽  
Drew Weingarth ◽  
Myrna E. Trumbauer ◽  
Dawn E. Novi ◽  
...  
Keyword(s):  
Body Weight ◽  
Neuropeptide Y ◽  
Energy Homeostasis ◽  
Arcuate Nucleus ◽  
Body Weight Gain ◽  
Physiological Role ◽  
Related Protein ◽  
Double Knockout ◽  
Orexigenic Peptide ◽  
Agouti Related Protein

ABSTRACT Agouti-related protein (AgRP), a neuropeptide abundantly expressed in the arcuate nucleus of the hypothalamus, potently stimulates feeding and body weight gain in rodents. AgRP is believed to exert its effects through the blockade of signaling by α-melanocyte-stimulating hormone at central nervous system (CNS) melanocortin-3 receptor (Mc3r) and Mc4r. We generated AgRP-deficient (Agrp−/− ) mice to examine the physiological role of AgRP. Agrp−/− mice are viable and exhibit normal locomotor activity, growth rates, body composition, and food intake. Additionally, Agrp−/− mice display normal responses to starvation, diet-induced obesity, and the administration of exogenous leptin or neuropeptide Y (NPY). In situ hybridization failed to detect altered CNS expression levels for proopiomelanocortin, Mc3r, Mc4r, or NPY mRNAs in Agrp−/− mice. As AgRP and the orexigenic peptide NPY are coexpressed in neurons of the arcuate nucleus, we generated AgRP and NPY double-knockout (Agrp−/− ;Npy−/− ) mice to determine whether NPY or AgRP plays a compensatory role in Agrp−/− or NPY-deficient (Npy−/− ) mice, respectively. Similarly to mice deficient in either AgRP or NPY, Agrp−/− ;Npy−/− mice suffer no obvious feeding or body weight deficits and maintain a normal response to starvation. Our results demonstrate that neither AgRP nor NPY is a critically required orexigenic factor, suggesting that other pathways capable of regulating energy homeostasis can compensate for the loss of both AgRP and NPY.

scholarly journals Prominent pancreatic endocrinopathy and altered control of food intake disrupt energy homeostasis in prion diseases

2008 ◽  
Vol 197 (2) ◽  
pp. 251-263 ◽  
Author(s):  
J D Bailey ◽  
J G Berardinelli ◽  
T E Rocke ◽  
R A Bessen
Keyword(s):  
Body Weight ◽  
Energy Homeostasis ◽  
Prion Diseases ◽  
Glucagon Secretion ◽  
Type Ii Diabetes Mellitus ◽  
Serum Glucose ◽  
Endocrine Function ◽  
Prion Infection ◽  
Control Food ◽  
Pancreatic Endocrine Function

Prion diseases are fatal neurodegenerative diseases that can induce endocrinopathies. The basis of altered endocrine function in prion diseases is not well understood, and the purpose of this study was to investigate the spatiotemporal relationship between energy homeostasis and prion infection in hamsters inoculated with either the 139H strain of scrapie agent, which induces preclinical weight gain, or the HY strain of transmissible mink encephalopathy (TME), which induces clinical weight loss. Temporal changes in body weight, feed, and water intake were measured as well as both non-fasted and fasted concentrations of serum glucose, insulin, glucagon, β-ketones, and leptin. In 139H scrapie-infected hamsters, polydipsia, hyperphagia, non-fasted hyperinsulinemia with hyperglycemia, and fasted hyperleptinemia were found at preclinical stages and are consistent with an anabolic syndrome that has similarities to type II diabetes mellitus and/or metabolic syndrome X. In HY TME-infected hamsters, hypodipsia, hypersecretion of glucagon (in both non-fasted and fasted states), increased fasted β-ketones, fasted hypoglycemia, and suppressed non-fasted leptin concentrations were found while feed intake was normal. These findings suggest a severe catabolic syndrome in HY TME infection mediated by chronic increases in glucagon secretion. In both models, alterations of pancreatic endocrine function were not associated with PrPSc deposition in the pancreas. The results indicate that prominent endocrinopathy underlies alterations in body weight, pancreatic endocrine function, and intake of food. The prion-induced alterations of energy homeostasis in 139H scrapie- or HY TME-infected hamsters could occur within areas of the hypothalamus that control food satiety and/or within autonomic centers that provide neural outflow to the pancreas.

scholarly journals Exercise alters the mitochondrial proteostasis and induces the mitonuclear imbalance and UPRmt in the hypothalamus of mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Renata R. Braga ◽  
Barbara M. Crisol ◽  
Rafael S. Brícola ◽  
Marcella R. Sant’ana ◽  
Susana C. B. R. Nakandakari ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Body Weight ◽  
Physical Training ◽  
Energy Homeostasis ◽  
Mitochondrial Activity ◽  
In Vivo Experiments ◽  
Reduced Body ◽  
Hypothalamic Cells ◽  
Bxd Mice

AbstractThe maintenance of mitochondrial activity in hypothalamic neurons is determinant to the control of energy homeostasis in mammals. Disturbs in the mitochondrial proteostasis can trigger the mitonuclear imbalance and mitochondrial unfolded protein response (UPRmt) to guarantee the mitochondrial integrity and function. However, the role of mitonuclear imbalance and UPRmt in hypothalamic cells are unclear. Combining the transcriptomic analyses from BXD mice database and in vivo experiments, we demonstrated that physical training alters the mitochondrial proteostasis in the hypothalamus of C57BL/6J mice. This physical training elicited the mitonuclear protein imbalance, increasing the mtCO-1/Atp5a ratio, which was accompanied by high levels of UPRmt markers in the hypothalamus. Also, physical training increased the maximum mitochondrial respiratory capacity in the brain. Interestingly, the transcriptomic analysis across several strains of the isogenic BXD mice revealed that hypothalamic mitochondrial DNA-encoded genes were negatively correlated with body weight and several genes related to the orexigenic response. As expected, physical training reduced body weight and food intake. Interestingly, we found an abundance of mt-CO1, a mitochondrial DNA-encoded protein, in NPY-producing neurons in the lateral hypothalamus nucleus of exercised mice. Collectively, our data demonstrated that physical training altered the mitochondrial proteostasis and induced the mitonuclear protein imbalance and UPRmt in hypothalamic cells.

scholarly journals Neonatal nutritional programming impairs adiponectin effects on energy homeostasis in adult life of male rats

2018 ◽  
Vol 315 (1) ◽  
pp. E29-E37 ◽  
Author(s):  
Mariana Peduti Halah ◽  
Paula Beatriz Marangon ◽  
Jose Antunes-Rodrigues ◽  
Lucila L. K. Elias
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Food Intake ◽  
White Adipose Tissue ◽  
Energy Homeostasis ◽  
Body Weight Gain ◽  
Adult Life ◽  
Male Rats ◽  
Nutritional Programming

Neonatal nutritional changes induce long-lasting effects on energy homeostasis. Adiponectin influences food intake and body weight. The aim of this study was to investigate the effects of neonatal nutritional programming on the central stimulation of adiponectin. Male Wistar rats were divided on postnatal (PN) day 3 in litters of 3 (small litter, SL), 10 (normal litter, NL), or 16 pups/dam (large litter, LL). We assessed body weight gain for 60 days, adiponectin concentration, and white adipose tissue weight. We examined the response of SL, NL, and LL rats on body weight gain, food intake, oxygen consumption (V̇o2), respiratory exchange ratio (RER), calorimetry, locomotor activity, phosphorylated-AMP-activated protein kinase (AMPK) expression in the hypothalamus, and uncoupling protein (UCP)-1 in the brown adipose tissue after central stimulus with adiponectin. After weaning, SL rats maintained higher body weight gain despite similar food intake compared with NL rats. LL rats showed lower body weight at weaning, with a catch up afterward and higher food intake. Both LL and SL groups had decreased plasma concentrations of adiponectin at PN60. SL rats had increased white adipose tissue. Central injection of adiponectin decreased body weight and food intake and increased V̇o2, RER, calorimetry, p-AMPK and UCP- 1 expression in NL rats, but it had no effect on SL and LL rats, compared with the respective vehicle groups. In conclusion, neonatal under- and overfeeding induced an increase in body weight gain in juvenile and early adult life. Unresponsiveness to central effects of adiponectin contributes to the imbalance of the energy homeostasis in adult life induced by neonatal nutritional programming.

scholarly journals Medical and non-medical complications among children and adolescents with excessive body weight

2014 ◽  
Vol 14 (1) ◽  
Author(s):  
Albane BR Maggio ◽  
Xavier E Martin ◽  
Catherine Saunders Gasser ◽  
Claudine Gal-Duding ◽  
Maurice Beghetti ◽  
...  
Keyword(s):  
Body Weight ◽  
Children And Adolescents ◽  
Medical Complications ◽  
Excessive Body Weight

Defense of differfing body weight set points in diet-induced obese and resistant rats

1998 ◽  
Vol 274 (2) ◽  
pp. R412-R419 ◽  
Author(s):  
Barry E. Levin ◽  
Richard E. Keesey
Keyword(s):  
Body Weight ◽  
Diet Composition ◽  
Energy Homeostasis ◽  
Energy Content ◽  
Sprague Dawley ◽  
Fat Pad ◽  
Insulin Levels ◽  
Diet Induced Obesity ◽  
Sprague Dawley Rats ◽  
Plasma Leptin

Among outbred Sprague-Dawley rats, approximately one-half develop diet-induced obesity (DIO) and one-half are diet resistant (DR) on a diet relatively high in fat and energy content (HE diet). Here we examined the defense of body weight in these two phenotypes. After HE diet for 13 wk, followed by chow for 6 wk, DR rats gained weight comparably but their plasma leptin levels fell to 54% of chow-fed controls. When a palatable liquid diet (Ensure) was added for 13 wk, other DR rats became obese. But when switched to chow, their intakes fell by 60%, and body and retroperitoneal (RP) fat pad weights and plasma leptin and insulin levels all declined for 2 wk and then stabilized at control levels after 6 wk. In contrast, comparably obese DIO rats decreased their intake by only 20%, and their weights plateaued when they were switched to chow after 13 wk on HE diet. When a subgroup of these DIO rats was restricted to 60% of prior intake, their weights fell to chow-fed control levels over 2 wk. But their leptin and insulin levels both fell disproportionately to 30% of controls. When no longer restricted, their intake and feed efficiency rose immediately, and their body and RP pad weights and leptin and insulin levels rose to those of unrestricted DIO rats within 2 wk. Thus diet and genetic background interact to establish high (DIO) or low (DR) body weight set points, which are then defended against subsequent changes in diet composition and/or energy availability. If leptin affects energy homeostasis, it does so differentially in DIO vs. DR rats since comparably low and high levels were associated with differing patterns of weight change between the two phenotypes.

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