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.

scholarly journals Deficiency of PTP1B in POMC neurons leads to alterations in energy balance and homeostatic response to cold exposure

2011 ◽  
Vol 300 (6) ◽  
pp. E1002-E1011 ◽  
Author(s):  
Bart C. De Jonghe ◽  
Matthew R. Hayes ◽  
Ryoichi Banno ◽  
Karolina P. Skibicka ◽  
Derek J. Zimmer ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Energy Balance ◽  
Food Intake ◽  
Cold Exposure ◽  
Tyrosine Phosphatase ◽  
Negative Regulator ◽  
Leptin Signaling ◽  
Leptin Sensitivity ◽  
Brown Adipose

The adipose tissue-derived hormone leptin regulates energy balance through catabolic effects on central circuits, including proopiomelanocortin (POMC) neurons. Leptin activation of POMC neurons increases thermogenesis and locomotor activity. Protein tyrosine phosphatase 1B (PTP1B) is an important negative regulator of leptin signaling. POMC neuron-specific deletion of PTP1B in mice results in reduced high-fat diet-induced body weight and adiposity gain due to increased energy expenditure and greater leptin sensitivity. Mice lacking the leptin gene ( ob/ob mice) are hypothermic and cold intolerant, whereas leptin delivery to ob/ob mice induces thermogenesis via increased sympathetic activity to brown adipose tissue (BAT). Here, we examined whether POMC PTP1B mediates the thermoregulatory response of CNS leptin signaling by evaluating food intake, body weight, core temperature (TC), and spontaneous physical activity (SPA) in response to either exogenous leptin or 4-day cold exposure (4°C) in male POMC-Ptp1b-deficient mice compared with wild-type controls. POMC-Ptp1b −/− mice were hypersensitive to leptin-induced food intake and body weight suppression compared with wild types, yet they displayed similar leptin-induced increases in TC. Interestingly, POMC-Ptp1b −/− mice had increased BAT weight and elevated plasma triiodothyronine (T3) levels in response to a 4-day cold challenge, as well as reduced SPA 24 h after cold exposure, relative to controls. These data show that PTP1B in POMC neurons plays a role in short-term cold-induced reduction of SPA and may influence cold-induced thermogenesis via enhanced activation of the thyroid axis.

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 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 Deficiency of PTP1B in Leptin Receptor-Expressing Neurons Leads to Decreased Body Weight and Adiposity in Mice

Endocrinology ◽  
2012 ◽  
Vol 153 (9) ◽  
pp. 4227-4237 ◽  
Author(s):  
Ryan C. Tsou ◽  
Derek J. Zimmer ◽  
Bart C. De Jonghe ◽  
Kendra K. Bence
Keyword(s):  
Body Weight ◽  
Leptin Receptor ◽  
Body Weight Gain ◽  
Tyrosine Phosphatase ◽  
Negative Regulator ◽  
Metabolic Effects ◽  
Metabolic Phenotype ◽  
Leptin Signaling ◽  
Reduced Body ◽  
Leptin Sensitivity

Protein tyrosine phosphatase 1B (PTP1B) is a ubiquitously expressed tyrosine phosphatase implicated in the negative regulation of leptin and insulin receptor signaling. PTP1B−/− mice possess a lean metabolic phenotype attributed at least partially to improved hypothalamic leptin sensitivity. Interestingly, mice lacking both leptin and PTP1B (ob/ob:PTP1B−/−) have reduced body weight compared with mice lacking leptin only, suggesting that PTP1B may have important leptin-independent metabolic effects. We generated mice with PTP1B deficiency specifically in leptin receptor (LepRb)-expressing neurons (LepRb-PTP1B−/−) and compared them with LepRb-Cre-only wild-type (WT) controls and global PTP1B−/− mice. Consistent with PTP1B's role as a negative regulator of leptin signaling, our results show that LepRb-PTP1B−/− mice are leptin hypersensitive and have significantly reduced body weight when maintained on chow or high-fat diet (HFD) compared with WT controls. LepRb-PTP1B−/− mice have a significant decrease in adiposity on HFD compared with controls. Notably, the extent of attenuated body weight gain on HFD, as well as the extent of leptin hypersensitivity, is similar between LepRb-PTP1B−/− mice and global PTP1B−/− mice. Overall, these results demonstrate that PTP1B deficiency in LepRb-expressing neurons results in reduced body weight and adiposity compared with WT controls and likely underlies the improved metabolic phenotype of global and brain-specific PTP1B-deficient models. Subtle phenotypic differences between LepRb-PTP1B−/− and global PTP1B−/− mice, however, suggest that PTP1B independent of leptin signaling may also contribute to energy balance in mice.

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.

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