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Increased beta -oxidation but no insulin resistance or glucose intolerance in mice lacking adiponectin
Ke Ma1, Agatha Cabrero, Pradip K Saha
1Section of Endocrinology & Metabolism, Department of Medicine, Baylor College of Medicine and the St. Luke's Episcopal Hospital, Texas Medical Center, Houston, Texas 77030, USA.
Abstract:
Previous reports showed that recombinant fragments of adiponectin (adipo) displayed pharmacological effects when injected into rodents, but the relevance of these observations to the physiological function of adipo is unclear. We generated Adipo(-/-) mice by gene targeting. Adipo(-/-) mice are fertile with normal body and fat pad weights. Plasma glucose and insulin levels of Adipo(-/-) and Adipo(+/+) mice are similar under fasting conditions and during an intraperitoneal glucose tolerance test (GTT). Insulin tolerance test (ITT) also produces similar plasma glucose and insulin levels in the two groups of mice. Hyperinsulinemic-euglycemic clamp analysis showed that Adipo(-/-) and Adipo(+/+) mice have similar glucose infusion rates to maintain a similar serum glucose. High-fat diet feeding for 7 months led to similar weight gain and similar GTT and ITT responses. We next measured beta-oxidation and found it to be significantly increased in muscle and liver of Adipo(-/-) mice. In conclusion, our study indicates that absence of adipo causes increased beta-oxidation but does not cause glucose intolerance or insulin resistance in mice.
Insights
Mice lacking adiponectin (adipo) show increased fat breakdown (beta-oxidation) but maintain normal glucose and insulin levels. This suggests adiponectin is not essential for glucose homeostasis in mice.
Area of Science:
- Metabolism
- Endocrinology
- Genetics
Background:
- Recombinant adiponectin fragments show pharmacological effects in rodents.
- The physiological role of adiponectin in vivo remains unclear.
Purpose of the Study:
- To investigate the physiological function of adiponectin.
- To determine the impact of adiponectin absence on glucose metabolism and insulin sensitivity.
Main Methods:
- Generated adiponectin-deficient (Adipo-/-) mice using gene targeting.
- Performed glucose tolerance tests (GTT) and insulin tolerance tests (ITT).
- Conducted hyperinsulinemic-euglycemic clamp analysis and measured beta-oxidation.
Main Results:
- Adipo-/- mice exhibited normal fertility, body weight, and fat pad weights.
- No significant differences in plasma glucose or insulin levels were observed between Adipo-/- and wild-type mice under various conditions.
- Absence of adiponectin led to significantly increased beta-oxidation in muscle and liver tissues.
- High-fat diet did not induce glucose intolerance or insulin resistance in Adipo-/- mice.
Conclusions:
- Adiponectin deficiency increases beta-oxidation in mice.
- Adiponectin is not essential for maintaining glucose tolerance or insulin sensitivity in mice.