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Updated: Jul 21, 2026
08:13
Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT)
Published on: January 7, 2018
Plasma leptin concentrations do not appear to decrease insulin-mediated glucose disposal or glucose-stimulated
M Carantoni1, F Abbasi, S Azhar
1Stanford University School of Medicine, California, USA.
Diabetes
|March 31, 1998
Summary
This study found that higher leptin levels in women with normal glucose tolerance were linked to insulin resistance, but not directly to impaired insulin secretion or action. The findings suggest leptin may increase secondary to insulin resistance, rather than causing it.
Area of Science:
- Endocrinology
- Metabolic Syndrome
- Obesity Research
Background:
- Leptin, a hormone produced by adipose tissue, plays a role in regulating energy balance and appetite.
- Its potential contribution to the pathophysiology of non-insulin-dependent diabetes mellitus (NIDDM) is debated, particularly concerning its effects on insulin sensitivity and secretion.
- Understanding leptin's role is crucial for developing targeted therapies for metabolic disorders.
Purpose of the Study:
- To investigate the hypothesis that plasma leptin concentrations contribute to NIDDM pathophysiology by reducing insulin-mediated glucose disposal and glucose-stimulated insulin secretion.
- To determine the independent relationship between leptin levels, insulin action, and insulin secretion in women with normal oral glucose tolerance.
Main Methods:
- Study involved 60 women with normal oral glucose tolerance.
- Insulin-mediated glucose disposal was assessed by steady-state plasma glucose (SSPG) during a 180-min infusion of somatostatin, glucose, and insulin.
- Glucose-stimulated insulin secretion was measured by the incremental increase in insulin concentration (deltaIns) post-oral glucose challenge.
Main Results:
- Higher fasting plasma leptin concentrations correlated positively with insulin resistance (higher SSPG).
- This association was independent of age and BMI, but disappeared when total insulin response was accounted for.
- Leptin showed a positive correlation with deltaIns, contrary to the expected inhibitory effect on insulin secretion. The relationship between deltaIns and SSPG was confirmed, but not between deltaIns and leptin.
Conclusions:
- Circulating leptin does not appear to have a primary detrimental effect on insulin action or secretion in women with normal glucose tolerance.
- Elevated leptin concentrations in insulin-resistant individuals may be a consequence of chronic hyperinsulinemia stimulating leptin production.
- Further research is needed to elucidate the complex interplay between leptin, insulin resistance, and NIDDM pathogenesis.
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