Related Experiment Video
Updated: Jul 26, 2026
09:20
An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA Modulation on Adipocyte Function
Published on: May 4, 2021
Leptin, insulin and TNF-alpha in weight loss
C Xenachis1, E Samojlik, M P Raghuwanshi
1Division of Endocrinology, Diabetes and Metabolism, UMDNJ, New Jersey Medical School, Newark 07103, USA.
Journal of Endocrinological Investigation
|January 31, 2002
Summary
Serum leptin, insulin, and tumor necrosis factor-alpha decreased during a 10-week weight loss program. However, their variable changes mean they are not reliable markers for tracking weekly weight loss compliance.
Area of Science:
- Metabolism and Endocrinology
- Obesity Research
- Biomarker Discovery
Background:
- Morbid obesity presents significant health challenges.
- Effective weight loss strategies are crucial for improving patient outcomes.
- Identifying reliable biomarkers for monitoring weight loss compliance is an ongoing research area.
Purpose of the Study:
- To investigate the utility of serum leptin as a marker for weight loss compliance in morbidly obese patients.
- To compare the changes in serum leptin, insulin, and tumor necrosis factor-alpha (TNF-alpha) during a structured weight loss program.
Main Methods:
- Forty-eight morbidly obese patients participated in a 10-week, 800 kcal/day formula diet (OPTIFAST) program.
- Weekly serum leptin levels were measured.
- In a subgroup, serial assessments of serum insulin and TNF-alpha were also conducted.
Main Results:
- Serum leptin decreased significantly in successful weight loss patients (13.6% loss, 50% leptin decrease) compared to non-successful patients (7.0% loss, 22% leptin decrease).
- Leptin changes showed only a two-thirds concordance with weekly weight loss.
- Serum insulin decreased more rapidly than leptin, while TNF-alpha changes were erratic (48% concordance).
Conclusions:
- Serum leptin, insulin, and TNF-alpha levels decrease with rapid weight loss.
- The differing rates and variability of these markers preclude their use as precise indicators of week-to-week weight loss compliance.
- Further research is needed to identify more reliable compliance biomarkers.
More Related Videos
Related Concept Videos
01:24Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF
Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab (Humira),...
01:30Regulation 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...
01:16Insulin: Dosing Regimen and Adverse Effects
Insulin-replacement therapy usually includes both long-acting insulin (basal) and short-acting insulin (to cater to postprandial needs). In a diverse group of type 1 diabetes patients, the average daily insulin dose is typically 0.5-0.7 units/kg body weight. However, obese patients and pubertal adolescents may need more due to insulin resistance.
The basal dose constitutes about 40%-50% of the total daily dose, with the rest as premeal insulin. The mealtime insulin dose should mirror...
The basal dose constitutes about 40%-50% of the total daily dose, with the rest as premeal insulin. The mealtime insulin dose should mirror...
01:24Glucagon-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...
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...
01:23Dipeptidyl Peptidase 4 Inhibitors
Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a significant...
01:26Type I Diabetes II: Pathophysiology
Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...