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Updated: Jul 7, 2026

Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance

Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance

Published on: February 17, 2023

Selective versus total insulin resistance: a pathogenic paradox.

Michael S Brown¹, Joseph L Goldstein

¹Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. mike.brown@utsouthwestern.edu <mike.brown@utsouthwestern.edu>

Cell Metabolism

|February 6, 2008

Summary

Mice with type 2 diabetes develop selective hepatic insulin resistance, causing hyperglycemia and hypertriglyceridemia. Total hepatic insulin resistance, however, results in hyperglycemia without hypertriglyceridemia, indicating a less severe condition.

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Area of Science:

Metabolic diseases
Endocrinology
Molecular biology

Background:

Type 2 diabetes is characterized by selective hepatic insulin resistance, where insulin cannot suppress glucose production but still promotes fat synthesis.
This selective resistance leads to detrimental hyperglycemia and hypertriglyceridemia in diabetic mice.

Discussion:

Biddinger et al. (2008) investigated the effects of total hepatic insulin resistance in mice.
Their findings reveal that complete insulin resistance in the liver paradoxically results in a less severe metabolic state than selective resistance.

Key Insights:

Mice with total hepatic insulin resistance display hyperglycemia but not hypertriglyceridemia.
This suggests that the ability of insulin to regulate lipogenesis is crucial for the development of hypertriglyceridemia in the context of insulin resistance.

Outlook:

Further research into the distinct molecular mechanisms governing hepatic gluconeogenesis and lipogenesis is warranted.
Understanding these pathways could lead to more targeted therapies for type 2 diabetes and related metabolic disorders.