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Updated: Apr 27, 2026

Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice
Published on: November 16, 2011
Insulin resistance in euglycemic cirrhosis
Amitava Goswami1, Narendra Bhargava1, Sunil Dadhich1
1Department of Gastroenterology, Dr Sampurnanand Medical College, Jodhpur, India.
Insulin resistance (IR) is common in cirrhosis, with pancreatic beta-cells compensating initially. Advanced liver disease can lead to impaired beta-cell function and hepatogenous diabetes.
Area of Science:
- Hepatology
- Endocrinology
- Metabolic Syndrome
Background:
- Insulin resistance (IR) is linked to hepatic fibrosis and cirrhosis.
- The mechanism of hyperinsulinemia in cirrhosis remains unclear.
- This study investigates hyperinsulinemia and pancreatic beta-cell function in euglycemic cirrhosis.
Purpose of the Study:
- To assess hyperinsulinemia and pancreatic beta-cell function in euglycemic cirrhosis of varied etiology.
- To evaluate the relationship between IR, cirrhosis severity, and beta-cell function.
Main Methods:
- Cross-sectional case-control study of 100 subjects.
- Insulin resistance assessed using Homeostasis Model Assessment (HOMA) and quantitative insulin sensitivity check index.
- Pancreatic beta-cell function evaluated via HOMA-beta in different cirrhosis stages.
Main Results:
- Overall IR observed in 68.5% of euglycemic cirrhosis patients.
- IR prevalence varied by etiology: Hepatitis C (100%), NAFLD (100%), Autoimmune Hepatitis (100%), HCC (80%), Alcoholic Liver Disease (72%), Hepatitis B (45%).
- Elevated HOMA-IR and HOMA-beta correlated with advanced cirrhosis (CTP score >9, MELD score >15). HOMA-beta was significantly higher in euglycemic cases compared to diabetic controls.
Conclusions:
- Insulin resistance is prevalent in euglycemic cirrhosis.
- Compensatory increase in pancreatic beta-cell insulin secretion occurs with advancing liver disease.
- Prolonged IR may lead to impaired beta-cell function and hepatogenous diabetes.
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