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Related Concept Videos

Regulation of Food Intake01:30

Regulation of Food Intake

Short-term regulation of food intake primarily involves neural signals from the gastrointestinal (GI) tract, blood nutrient levels, and GI tract hormones. Communication between the gut and brain via vagal nerve fibers plays a significant role in evaluating the contents of the gut. Clinical studies have shown that protein ingestion produces a more prolonged response in these nerve fibers compared to an equivalent amount of glucose. Additionally, the activation of stretch receptors caused by GI...
Glucagon-like Receptor Agonists01:24

Glucagon-like Receptor Agonists

Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by the...
Pharmacokinetics in Obese Patients: Drug Absorption and Distribution01:25

Pharmacokinetics in Obese Patients: Drug Absorption and Distribution

Obesity significantly alters the pharmacokinetic processes of drug absorption and distribution, presenting unique challenges in medical treatment. The increased fat tissue and decreased lean muscle in obese individuals can significantly affect how drugs are absorbed into the body and distributed across different tissues. This alteration can lead to variances in the effectiveness and safety of medications, necessitating adjustments in dosing or drug selection for obese patients.One notable...
Metabolic States of the Body: Fasting and Starvation01:24

Metabolic States of the Body: Fasting and Starvation

During the initial hours of fasting, the body uses up its glycogen stores as an energy source. Once these glycogen reserves are depleted, the body begins breaking down stored triglycerides and structural proteins. During this stage, glycerol becomes a key substrate for gluconeogenesis, while free fatty acids undergo beta-oxidation to provide energy for tissues, such as skeletal muscle. In the fasting state, the body spares protein breakdown as much as possible to conserve muscle and structural...
Hypoglycemia and Glucagon01:15

Hypoglycemia and Glucagon

Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
Pharmacokinetics in Obese Patients: Drug Metabolism and Excretion01:20

Pharmacokinetics in Obese Patients: Drug Metabolism and Excretion

Drug metabolism, a critical process in the liver, involves two primary phases: Phase I reactions and Phase II conjugation. Obesity introduces significant alterations in this metabolic process, primarily due to fatty infiltration of the liver, leading to conditions such as nonalcoholic fatty liver disease (NAFLD). This condition can modify the activities of both Phase I and II enzymes, impacting how drugs are metabolized in obese patients.Phase I metabolism sees variable effects across...

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Related Experiment Video

Updated: May 23, 2026

White and Brown Adipose Grafts: An Approach to Correct Reproductive, Metabolic, and Renal Deficits in Black and Tan Brachyury (BTBR) Obese Mice
06:16

White and Brown Adipose Grafts: An Approach to Correct Reproductive, Metabolic, and Renal Deficits in Black and Tan Brachyury (BTBR) Obese Mice

Published on: September 9, 2025

Leptin in anorexia and cachexia syndrome.

Diana R Engineer1, Jose M Garcia

  • 1Division of Diabetes, Endocrinology and Metabolism, Michael E DeBakey Veterans Affairs Medical Center, Houston, TX 77030, USA.

International Journal of Peptides
|April 21, 2012
PubMed
Summary

Leptin, a hormone regulating appetite, is altered in chronic diseases, contributing to anorexia-cachexia syndrome. Understanding leptin pathway changes is crucial for managing this condition.

Area of Science:

  • Endocrinology
  • Metabolism
  • Physiology

Background:

  • Leptin, secreted by adipocytes, regulates food intake and energy expenditure via hypothalamic pathways.
  • Caloric deprivation typically leads to compensatory increases in appetite and body weight.
  • Anorexia-cachexia syndrome in chronic diseases paradoxically lacks this compensatory response.

Purpose of the Study:

  • To review evidence on leptin pathway alterations in anorexia-cachexia syndrome.
  • To explore potential mechanisms linking leptin signaling and inflammation in chronic diseases.

Main Methods:

  • Literature review of studies on leptin, inflammation, and anorexia-cachexia syndrome.
  • Analysis of potential crosstalk between leptin and inflammatory signaling pathways.

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Related Experiment Videos

Last Updated: May 23, 2026

White and Brown Adipose Grafts: An Approach to Correct Reproductive, Metabolic, and Renal Deficits in Black and Tan Brachyury (BTBR) Obese Mice
06:16

White and Brown Adipose Grafts: An Approach to Correct Reproductive, Metabolic, and Renal Deficits in Black and Tan Brachyury (BTBR) Obese Mice

Published on: September 9, 2025

A RAPID Method for Blood Processing to Increase the Yield of Plasma Peptide Levels in Human Blood
11:36

A RAPID Method for Blood Processing to Increase the Yield of Plasma Peptide Levels in Human Blood

Published on: April 28, 2016

Experimental Approach to Examine Leptin Signaling in the Carotid Bodies and its Effects on Control of Breathing
05:45

Experimental Approach to Examine Leptin Signaling in the Carotid Bodies and its Effects on Control of Breathing

Published on: October 25, 2019

Main Results:

  • Leptin levels and signaling are dysregulated in chronic diseases associated with anorexia-cachexia.
  • Inflammatory signaling pathways may interfere with normal leptin function.
  • This interference may explain the lack of compensatory appetite increase and energy expenditure.

Conclusions:

  • Alterations in the leptin pathway, potentially influenced by inflammation, are implicated in anorexia-cachexia syndrome.
  • Further research into these mechanisms could reveal therapeutic targets for managing weight loss in chronic conditions.