Abstract

Obesity in childhood is the main determinant of whole body reduced insulin sensitivity. This association has been demonstrated in multiple adult and pediatric cohorts. The mechanistic link explaining this association is the pattern of lipid partitioning in the face of excess calories and energy surplus. A tight relation exists between typical lipid deposition patterns, specifically within the skeletal muscle and liver, as well as the intra-abdominal compartment and whole body insulin sensitivity. The impact of lipid deposition within insulin responsive tissues such as the liver and skeletal muscle relates to the ability of fatty acid derivates to inhibit elements of the insulin signal transduction pathway. Strengthening the relation of obesity and reduced insulin sensitivity are the observations that weight gain reduces insulin sensitivity while weight loss increases it. This manifests as the appearance of cardiovascular risk factor clustering with weight gain and its recovery in the face of weight loss. Both obesity per se, via the adipocytokine profile it induces, and low insulin sensitivity, are independent determinants of the adverse metabolic phenotype characteristic of the metabolic syndrome.

Highlights

  • Vardit Gepstein and Ram Weiss*Specialty section: This article was submitted to Pediatric Endocrinology, a section of the journal

  • All authors listed have made a substantial, direct and intellectual contribution to the work, and approved it for publication

  • Obesity in childhood is the main determinant of whole body reduced insulin sensitivity

Read more

Summary

Vardit Gepstein and Ram Weiss*

Specialty section: This article was submitted to Pediatric Endocrinology, a section of the journal

Frontiers in Endocrinology
Obesity and Metabolic Syndrome in Childhood
THE PATHOPHYSIOLOGY OF INSULIN RESISTANCE AND ITS RELATION TO LIPID PARTITIONING
RELATION OF OBESITY IN CHILDHOOD AND INSULIN RESISTANCE
SUMMARY
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.