scholarly journals Melanocortin 4 receptor signals at the neuronal primary cilium to control food intake and body weight

2021 ◽  
Vol 131 (9) ◽  
Author(s):  
Yi Wang ◽  
Adelaide Bernard ◽  
Fanny Comblain ◽  
Xinyu Yue ◽  
Christophe Paillart ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Primary Cilium ◽  
Melanocortin 4 Receptor ◽  
Control Food ◽  
Control Food Intake

scholarly journals TOXIC EFFECTS OF LARGE DOSE OF QUASSIN IN NORMAL AND DEPRIVED MICROFLORA RAT GROUPS

2021 ◽  
Vol 22 (1) ◽  
pp. 67-83
Author(s):  
Duraid A.Abbas ◽  
O.M.S. Al—Shaha,
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Water Intake ◽  
Daily Food ◽  
Daily Water Intake ◽  
Control Food ◽  
Liver And Kidney ◽  
Daily Water ◽  
Control Food Intake ◽  
Intake Water

Eighteen rats were divided into three equal groups. The first group was closed orally with quassin, the second group was dosed with quassin after the gut flora were suppressed by difierent antibiotics, and the third group was served as a control. Food intake, water intake, and change in body weight were measured daily before dosing, during two weeks of dosing, and during one week after stopping dosing. Two eats from each group were killed at the end of each week, and stomach, liver, and kidney were collected for histopathologic examination. The results show a significant decline in daily food intake and daily change in body weight, and a significant increase in daily water intake in both dosed groups during the dosing period. Microscopic lesions were seen in the kidneys of both dosed rats group killed at the end of first and second week

scholarly journals Central and peripheral control of food intake

2017 ◽  
Vol 51 (1) ◽  
pp. 52-70 ◽  
Author(s):  
M. M. I. Abdalla
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Energy Expenditure ◽  
Current Knowledge ◽  
The Body ◽  
Therapeutic Implications ◽  
New Therapeutic Approaches ◽  
Control Food ◽  
Adiposity Signals ◽  
Control Food Intake

Abstract The maintenance of the body weight at a stable level is a major determinant in keeping the higher animals and mammals survive. Th e body weight depends on the balance between the energy intake and energy expenditure. Increased food intake over the energy expenditure of prolonged time period results in an obesity. Th e obesity has become an important worldwide health problem, even at low levels. The obesity has an evil effect on the health and is associated with a shorter life expectancy. A complex of central and peripheral physiological signals is involved in the control of the food intake. Centrally, the food intake is controlled by the hypothalamus, the brainstem, and endocannabinoids and peripherally by the satiety and adiposity signals. Comprehension of the signals that control food intake and energy balance may open a new therapeutic approaches directed against the obesity and its associated complications, as is the insulin resistance and others. In conclusion, the present review summarizes the current knowledge about the complex system of the peripheral and central regulatory mechanisms of food intake and their potential therapeutic implications in the treatment of obesity.

Safety Assessment ofLactobacillus fermentumCECT5716, a probiotic strain isolated from human milk

2009 ◽  
Vol 76 (2) ◽  
pp. 216-221 ◽  
Author(s):  
Federico Lara-Villoslada ◽  
Saleta Sierra ◽  
María Paz Díaz-Ropero ◽  
Juan Miguel Rodríguez ◽  
Jordi Xaus ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Oral Administration ◽  
Human Milk ◽  
Bacterial Translocation ◽  
Probiotic Strain ◽  
Oxidative Markers ◽  
Control Food ◽  
Stress Oxidative ◽  
Control Food Intake

Lactobacillus fermentumCECT5716, a probiotic strain isolated from human milk, was characterized in a previous study. The objective of this study was to evaluate its sensitivity to antibiotics and its potential toxicity and translocation ability after oral administration to mice. For this puropose, 40 Balb/C mice were divided in two groups (n=20 per group). One group was treated orally with 1010colony forming units (cfu)/mouse/day ofLb. fermentumCECT5716 during 28 d. The other group only received the excipient and was used as control. Food intake, body weight, bacterial translocation and different biochemical and haematological parameters were analysed. Oral administration ofLb. fermentumCECT5716 to mice had no adverse effects on mice. There were no significant differences in body weight or food intake between control and probiotic-treated mice. No bacteraemia was observed and there was no treatment-associated bacterial translocation to liver or spleen. Stress oxidative markers were not different in control and probiotic-treated mice. These results suggest that the strainLb. fermentumCECT5716 is non-pathogenic for mice even in doses 10,000 times higher (expressed per kg of body weight) than those normally consumed by humans.

scholarly journals Minireview: From Anorexia to Obesity—The Yin and Yang of Body Weight Control

Endocrinology ◽  
2003 ◽  
Vol 144 (9) ◽  
pp. 3749-3756 ◽  
Author(s):  
Jeffrey M. Zigman ◽  
Joel K. Elmquist
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Body Weight ◽  
Food Intake ◽  
Weight Control ◽  
Public Health Goal ◽  
Control Food ◽  
Control Body ◽  
Body Weight Control ◽  
Control Food Intake

Abstract Over the past decade, there has been a tremendous increase in the understanding of the molecular and neural mechanisms that control food intake and body weight. Yet eating disorders and cachexia are still common, and obesity cases are rising at alarming rates. Thus, despite recent progress, an increased understanding of the molecular and neural substrates that control body weight homeostasis is a major public health goal. In this review, we discuss the mechanisms by which metabolic signals interact with key behavioral, neuroendocrine, and autonomic regulatory regions of the central nervous system. Additionally, we offer a model in which hormones such as leptin and ghrelin interact with similar central nervous system circuits and engage them in such a way as to maintain an appropriate and tight regulation of body weight and food intake. Our model predicts that overstimulation or understimulation of these central pathways can result in obesity, anorexia, or cachexia.

scholarly journals Food intake reductions and increases in energetic responses by hindbrain leptin and melanotan II are enhanced in mice with POMC-specific PTP1B deficiency

2012 ◽  
Vol 303 (5) ◽  
pp. E644-E651 ◽  
Author(s):  
Bart C. De Jonghe ◽  
Matthew R. Hayes ◽  
Derek J. Zimmer ◽  
Scott E. Kanoski ◽  
Harvey J. Grill ◽  
...  
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Food Intake ◽  
Tyrosine Phosphatase ◽  
Negative Regulator ◽  
Melanocortin Receptor ◽  
Leptin Sensitivity ◽  
Control Food ◽  
Control Food Intake ◽  
Melanotan Ii

Leptin regulates energy balance through central circuits that control food intake and energy expenditure, including proopiomelanocortin (POMC) neurons. POMC neuron-specific deletion of protein tyrosine phosphatase 1B (PTP1B) ( Ptpn1 loxP/loxP POMC-Cre), a negative regulator of CNS leptin signaling, results in resistance to diet-induced obesity and improved peripheral leptin sensitivity in mice, thus establishing PTP1B as an important component of POMC neuron regulation of energy balance. POMC neurons are expressed in the pituitary, the arcuate nucleus of the hypothalamus (ARH), and the nucleus of the solitary tract (NTS) in the hindbrain, and it is unknown how each population might contribute to the phenotype of POMC-Ptp1b −/− mice. It is also unknown whether improved leptin sensitivity in POMC-Ptp1b −/− mice involves altered melanocortin receptor signaling. Therefore, we examined the effects of hindbrain administration (4th ventricle) of leptin (1.5, 3, and 6 μg) or the melanocortin 3/4R agonist melanotan II (0.1 and 0.2 nmol) in POMC-Ptp1b −/− (KO) and control PTP1Bfl/fl (WT) mice on food intake, body weight, spontaneous physical activity (SPA), and core temperature (TC). The results show that KO mice were hypersensitive to hindbrain leptin- and MTII-induced food intake and body weight suppression and SPA compared with WT mice. Greater increases in leptin- but not MTII-induced TC were also observed in KO vs. WT animals. In addition, KO mice displayed elevated hindbrain and hypothalamic MC4R mRNA expression. These studies are the first to show that hindbrain administration of leptin or a melanocortin receptor agonist alters energy balance in mice likely via participation of hindbrain POMC neurons.

Parenteral nutrition, brain glycogen, and food intake

1993 ◽  
Vol 265 (6) ◽  
pp. R1387-R1391
Author(s):  
M. M. Meguid ◽  
J. L. Beverly ◽  
Z. J. Yang ◽  
J. R. Gleason ◽  
R. A. Meguid ◽  
...  
Keyword(s):  
Food Intake ◽  
Parenteral Nutrition ◽  
Plasma Glucose ◽  
Glycogen Content ◽  
Fischer 344 Rats ◽  
Brain Glycogen ◽  
Fischer 344 ◽  
Control Food ◽  
Control Food Intake ◽  
Infusion Period

To determine whether brain glycogen concentrations change during parenteral nutrition, Fischer 344 rats with jugular vein catheters received 0.9 N saline or parenteral nutrition providing 100% of daily calories (PN-100). Rats were killed after 4 days of PN-100 and serially after PN-100 was stopped. Food intake decreased during PN-100 to approximately 15% of control, but total kilocalories eaten and infused over the 4-day PN-100 period was approximately 130% of control. Food intake of PN-100 rats remained low for 3-4 days post-PN-100. At the end of the 4-day PN-100 period, plasma glucose and insulin (P = 0.01) and whole brain glycogen (P < 0.005) were higher than but similar to control within 24 h of PN-100 being stopped. When PN-100 rats were not allowed to eat during the infusion period, plasma glucose was lower, plasma insulin higher, and brain glycogen content the same as in control rats after 4 days of PN-100. The increased brain glycogen was the likely consequence of the hyperglycemia and hyperinsulinemia during PN-100 and was not causally associated with the reduced food intake either during or immediately after PN-100.

scholarly journals Peptide YY, appetite and food intake

2005 ◽  
Vol 64 (2) ◽  
pp. 213-216 ◽  
Author(s):  
C. W. le Roux ◽  
S. R. Bloom
Keyword(s):  
Food Intake ◽  
Peptide Yy ◽  
Energy Content ◽  
Peak Plasma ◽  
Evolutionary Relationship ◽  
Gut Hormones ◽  
Amino Acid Peptide ◽  
Control Food ◽  
Glucagon Like Peptide 1 ◽  
Control Food Intake

Obesity is taking on pandemic proportions. The laws of thermodynamics, however, remain unchanged, as energy will be stored if less energy is expended than consumed; the storage is usually in the form of adipose tissue. Several neural, humeral and psychological factors control the complex process known as appetite. Recently, a close evolutionary relationship between the gut and brain has become apparent. The gut hormones regulate important gastrointestinal functions such as motility, secretion, absorption, provide feedback to the central nervous system on availability of nutrients and may play a part in regulating food intake. Peptide YY (PYY) is a thirty-six amino acid peptide related to neuropeptide Y (NPY) and is co-secreted with glucagon-like peptide 1. Produced by the intestinal L-cells, the highest tissue concentrations of PYY are found in distal segments of the gastrointestinal tract, although it is present throughout the gut. Following food intake PYY is released into the circulation. PYY concentrations are proportional to meal energy content and peak plasma levels appear postprandially after 1 h. PYY3-36 is a major form of PYY in both the gut mucosal endocrine cells and the circulation. Peripheral administration of PYY3-36 inhibits food intake for several hours in both rodents and man. The binding of PYY3-36 to the Y2 receptor leads to an inhibition of the NPY neurones and a possible reciprocal stimulation of the pro-opiomelanocortin neurones. Thus, PYY3-36 appears to control food intake by providing a powerful feedback on the hypothalamic circuits. The effect on food intake has been demonstrated at physiological concentrations and, therefore, PYY3-36 may be important in the everyday regulation of food intake.

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