The Role of the Thyroid and Food Intake in the Ageing of Collagen Fibres

Gerontology ◽  
1967 ◽  
Vol 13 (2) ◽  
pp. 65-69 ◽  
Author(s):  
J.S. Giles ◽  
A.V. Everitt
Keyword(s):  
Food Intake ◽  
Collagen Fibres

The Role of the Thyroid and Food Intake in the Ageing of Collagen Fibres

Gerontology ◽  
1969 ◽  
Vol 15 (6) ◽  
pp. 366-373 ◽  
Author(s):  
A.V. Everitt ◽  
J.S. Giles ◽  
A. Gal
Keyword(s):  
Food Intake ◽  
Collagen Fibres

scholarly journals Gastric Sensory and Motor Functions and Energy Intake in Health and Obesity—Therapeutic Implications

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1158
Author(s):  
Lizeth Cifuentes ◽  
Michael Camilleri ◽  
Andres Acosta
Keyword(s):  
Energy Consumption ◽  
Gastric Emptying ◽  
Food Intake ◽  
Gastric Volume ◽  
Obesity Management ◽  
Bariatric Endoscopy ◽  
Motor Functions ◽  
Therapeutic Implications ◽  
Intestinal Functions

Sensory and motor functions of the stomach, including gastric emptying and accommodation, have significant effects on energy consumption and appetite. Obesity is characterized by energy imbalance; altered gastric functions, such as rapid gastric emptying and large fasting gastric volume in obesity, may result in increased food intake prior to reaching usual fullness and increased appetite. Thus, many different interventions for obesity, including different diets, anti-obesity medications, bariatric endoscopy, and surgery, alter gastric functions and gastrointestinal motility. In this review, we focus on the role of the gastric and intestinal functions in food intake, pathophysiology of obesity, and obesity management.

scholarly journals SAT-604 The Role of the Focal Adhesion Kinase Family in Leptin Receptor Signaling

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Colleen Hadley ◽  
Isin Cakir ◽  
Roger D Cone
Keyword(s):  
Food Intake ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Leptin Receptor ◽  
Kinase Activity ◽  
Cytokine Receptor ◽  
Receptor Signaling ◽  
Kinase Family ◽  
Stat3 Phosphorylation

Abstract Overweight and obesity are global concerns affecting nearly one third of the world population. These conditions are characterized by increased adiposity and are accompanied by a proportional increase in circulating leptin, an anorexigenic adipokine. Leptin is responsible for signaling peripheral energy status to the central nervous system to modulate food intake and energy expenditure. As such, neurons within the hypothalamus expressing the long isoform of leptin receptor (LepRb), a type I cytokine receptor, are primarily responsible for mediating the effects of leptin, which signal predominantly through the JAK2-STAT3 transduction mechanism. STAT3 is a latent transcription factor activated upon phosphorylation, which triggers its homodimerization and nuclear translocation. Evidence, however, for JAK2-independent, STAT3-dependent leptin receptor signaling mechanisms exist. FAK (focal adhesion kinase, Ptk2) and Pyk2 (protein tyrosine kinase 2b, Ptk2b) are a subset of nonreceptor protein tyrosine kinases and comprise the focal adhesion kinase family. FAK and Pyk2 are implicated in the regulation of cytokine receptor signaling. Furthermore, Pyk2 knockout mice have an obesity prone phenotype. Here, we studied the role of the focal adhesion kinases in leptin receptor signaling using genetic and pharmacological approaches. We found that overexpression of Pyk2 or FAK increased STAT3 phosphorylation (activation). Overexpression of a FAK or Pyk2 construct with impaired kinase activity, however, attenuated STAT3 phosphorylation, suggesting the increase in STAT3 phosphorylation is largely dependent upon kinase activity of FAK/Pyk2. Treatment of cells with a small molecule dual inhibitor of FAK and Pyk2 (PF431396) attenuated leptin-induced STAT3 phosphorylation in a mouse hypothalamic cell line. Importantly, this effect is independent of JAK2, as PF treatment of two independent JAK2-deficient cell lines exhibited similar attenuation of leptin-induced STAT3 phosphorylation. To assess the physiological relevance of FAK/Pyk2 in leptin receptor signaling in vivo, we administered PF compound to the lateral ventricle of 24-hour fasted lean wild-type mice followed by peripheral leptin administration. Intracerebroventricular (ICV) administration of PF suppressed the anorectic effect of leptin as evidenced by impaired inhibition of food intake upon refeeding. Accordingly, analysis of total hypothalamic lysates from these mice showed ICV PF impaired leptin-induced STAT3 phosphorylation. Taken together, these data suggest that Pyk2 and/or FAK play a role in leptin signal transduction.

scholarly journals Role of Ventromedial Hypothalamus in Sucrose-Induced Obesity on Metabolic Parameters

2021 ◽  
pp. 097275312110057
Author(s):  
Archana Gaur ◽  
G.K. Pal ◽  
Pravati Pal
Keyword(s):  
Insulin Resistance ◽  
Weight Gain ◽  
Food Intake ◽  
Ventromedial Hypothalamus ◽  
Female Rats ◽  
Metabolic Parameters ◽  
Male Rats ◽  
Significant Weight Gain ◽  
The Metabolic Syndrome

Background: Obesity is because of excessive fat accumulation that affects health adversely in the form of various diseases such as diabetes, hypertension, cardiovascular diseases, and many other disorders. Our Indian diet is rich in carbohydrates, and hence the sucrose-induced obesity is an apt model to mimic this. Ventromedial hypothalamus (VMH) is linked to the regulation of food intake in animals as well as humans. Purpose: To understand the role of VMHin sucrose-induced obesity on metabolic parameters. Methods: A total of 24 adult rats were made obese by feeding them on a 32% sucrose solution for 10 weeks. The VMH nucleus was ablated in the experimental group and sham lesions were made in the control group. Food intake, body weight, and biochemical parameters were compared before and after the lesion. Results: Male rats had a significant weight gain along with hyperphagia, whereas female rats did not have a significant weight gain inspite of hyperphagia. Insulin resistance and dyslipidemia were seen in both the experimental and control groups. Conclusion: A sucrose diet produces obesity which is similar to the metabolic syndrome with insulin resistance and dyslipidemia, and a VMH lesion further exaggerates it. Males are more prone to this exaggeration.

scholarly journals Assessing the role of the growth hormone secretagogue receptor in motivational learning and food intake.

2009 ◽  
Vol 123 (5) ◽  
pp. 1058-1065 ◽  
Author(s):  
Alexander W. Johnson ◽  
Rebecca Canter ◽  
Michela Gallagher ◽  
Peter C. Holland
Keyword(s):  
Growth Hormone ◽  
Food Intake ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue

LPS inhibits fasted plasma ghrelin levels in rats: role of IL-1 and PGs and functional implications

2006 ◽  
Vol 291 (4) ◽  
pp. G611-G620 ◽  
Author(s):  
Lixin Wang ◽  
Nicole R. Basa ◽  
Almaas Shaikh ◽  
Andrew Luckey ◽  
David Heber ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Gastric Emptying ◽  
Food Intake ◽  
Intravenous Injection ◽  
Plasma Levels ◽  
Inhibitory Action ◽  
Functional Implications ◽  
Urocortin 1 ◽  
Fasted Rats

LPS injected intraperitoneally decreases fasted plasma levels of ghrelin at 3 h postinjection in rats. We characterized the inhibitory action of LPS on plasma ghrelin and whether exogenous ghrelin restores LPS-induced suppression of food intake and gastric emptying in fasted rats. Plasma ghrelin and insulin and blood glucose were measured after intraperitoneal injection of LPS, intravenous injection of IL-1β and urocortin 1, and in response to LPS under conditions of blockade of IL-1 or CRF receptors by subcutaneous injection of IL-1 receptor antagonist (IL-1Ra) or astressin B, respectively, and prostaglandin (PG) synthesis by intraperitoneal indomethacin. Food intake and gastric emptying were measured after intravenous injection of ghrelin at 5 h postintraperitoneal LPS injection. LPS inhibited the elevated fasted plasma ghrelin levels by 47.6 ± 4.9%, 58.9 ± 3.3%, 74.4 ± 2.7%, and 48.9 ± 8.7% at 2, 3, 5, and 7 h postinjection, respectively, and values returned to preinjection levels at 24 h. Insulin levels were negatively correlated to those of ghrelin, whereas there was no significant correlation between glucose and ghrelin. IL-1Ra and indomethacin prevented the first 3-h decline in ghrelin levels induced by LPS, whereas astressin B did not. IL-1β inhibited plasma ghrelin levels, whereas urocortin 1 had no influence. Ghrelin injected intravenously prevented an LPS-induced 87% reduction of gastric emptying and 61% reduction of food intake. These data showed that IL-1 and PG pathways are part of the early mechanisms by which LPS suppresses fasted plasma ghrelin and that exogenous ghrelin can normalize LPS-induced-altered digestive functions.

Role of bombesin-related peptides in the control of food intake

Neuropeptides ◽  
1999 ◽  
Vol 33 (5) ◽  
pp. 376-386 ◽  
Author(s):  
Z. Merali ◽  
J. McIntosh ◽  
H. Anisman
Keyword(s):  
Food Intake
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