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Insulin clearance in obesity.

M Elena Valera Mora1, Antonino Scarfone, Menotti Calvani

  • 1Institute of Internal Medicine, Catholic University of Rome, Largo Agostino Gemelli 8, 00168 Rome, Italy. valeramora@virgilio.it

Journal of the American College of Nutrition
|December 20, 2003
PubMed
Summary

This paper explores how insulin is cleared from the body, focusing on changes in obesity. It explains that insulin degrading enzyme is the main system for breaking down insulin. The liver and kidneys are primary sites for insulin clearance. In obese individuals, the liver's ability to clear insulin is impaired. The kidneys show increased filtration rates and plasma flow. This suggests a state of renal vasodilation. Other tissues like muscle and adipocytes also participate in insulin metabolism. The study highlights the complex nature of insulin clearance and how obesity disrupts normal metabolic processes.

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Area of Science:

  • Endocrinology and metabolism
  • Renal physiology
  • Obesity research

Background:

Insulin clearance mechanisms remain partially understood. Established knowledge shows insulin degrading enzyme (IDE) plays a central role in breaking down insulin. Protein disulfide isomerase and cathepsin D also contribute to insulin metabolism. The liver and kidneys are primary organs for insulin clearance. In obesity, hyperinsulinemia and elevated free fatty acids are common. These factors may disrupt hepatic insulin clearance. Renal function changes in obesity include increased glomerular filtration rate and plasma flow. This paper addresses gaps in understanding how obesity alters insulin clearance pathways.

Purpose Of The Study:

This study aims to clarify insulin clearance mechanisms in obesity. It focuses on how hyperinsulinemia and free fatty acids affect hepatic insulin processing. The paper also examines renal changes in obese individuals. Researchers seek to determine if renal vasodilation impacts insulin filtration. They investigate whether multiple tissues beyond liver and kidney contribute to insulin clearance. The goal is to map how obesity disrupts normal insulin metabolism. This work builds on prior findings about IDE and protein disulfide isomerase roles. It addresses gaps in understanding tissue-specific insulin degradation.

Keywords:
Insulin metabolismObesity effectsRenal functionMetabolic pathways

Frequently Asked Questions

Obese individuals show impaired hepatic insulin clearance. Hyperinsulinemia and elevated free fatty acids likely contribute to this disruption.

Insulin degrading enzyme is the primary system. Protein disulfide isomerase and cathepsin D also participate in insulin metabolism.

The kidney filters insulin through glomerular filtration. In obesity, increased filtration rates suggest altered renal insulin processing.

Yes. Muscle, adipocytes, and gastrointestinal cells contain insulin receptors and participate in insulin metabolism.

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Main Methods:

The study reviews existing literature on insulin metabolism pathways. It analyzes the role of insulin degrading enzyme in insulin breakdown. Researchers examine how protein disulfide isomerase and cathepsin D function. They assess liver and kidney contributions to insulin clearance. The paper evaluates how obesity alters hepatic insulin processing. It investigates renal changes including filtration rates and plasma flow. The study also considers non-traditional tissues like muscle and adipocytes. Researchers use a systematic review approach to synthesize current evidence.

Main Results:

Insulin degrading enzyme is the primary system for insulin breakdown. The liver and kidneys are key sites for insulin clearance. In obesity, hepatic insulin clearance is impaired. Elevated free fatty acids may contribute to this impairment. Renal function in obesity shows increased glomerular filtration rate. Renal plasma flow and albumin excretion are also elevated. This suggests renal vasodilation in obese individuals. Multiple tissues including muscle and adipocytes participate in insulin metabolism.

Conclusions:

The authors suggest insulin clearance involves multiple tissues beyond liver and kidney. They propose that obesity disrupts hepatic insulin processing. The paper indicates renal vasodilation may affect insulin filtration. Researchers highlight the role of insulin degrading enzyme in insulin metabolism. They suggest protein disulfide isomerase and cathepsin D also contribute. The study emphasizes the complexity of insulin clearance pathways. The authors note that free fatty acids may impair hepatic insulin clearance. They conclude that obesity alters normal insulin metabolism through multiple mechanisms.

Obesity increases glomerular filtration rate and renal plasma flow. Albumin excretion also rises, suggesting renal vasodilation.

Impaired hepatic clearance in obesity may lead to higher insulin levels. This suggests a feedback loop between insulin levels and clearance efficiency.