Abstract
Adiponectin is an adipocyte-derived hormone that has a number of metabolic effects in the body, including the control of both glucose and fatty acid metabolism. The globular head domain of adiponectin, gAd, has also been shown to increase fatty acid oxidation in skeletal muscle. Within days after birth, a rapid increase in fatty acid oxidation occurs in the heart. We examined whether adiponectin or gAd plays a role in this maturation of cardiac fatty acid oxidation. Plasma adiponectin increased in newborn rabbits following birth: 1.2 +/- 0.3 microg/ml in 1-day-old, 6.8 +/- 1.8 microg/ml in 7-day-old, and 45 +/- 5 microg/ml in 6-week-old rabbits. Because plasma insulin levels decrease and remain low throughout the suckling period, and because this decrease may contribute to the maturation of fatty acid oxidation, we examined the effects of adiponectin and gAd on fatty acid oxidation in isolated perfused 1-day-old rabbit hearts in the presence or absence of 100 microunits/ml insulin. Adiponectin (10 microg/ml) did not alter fatty acid oxidation in the presence of insulin. In the absence of insulin, the addition of recombinant gAd (1.5 microg/ml) increased fatty acid oxidation compared with control (129 +/- 18 versus 66 +/- 11 nmol.g dry weight(-1).min(-1), respectively (p < 0.05). In 7-day-old hearts, where fatty acid oxidation rates were 5-fold higher than 1-day-old hearts, gAd did not alter fatty acid oxidation rates. The increase in fatty acid oxidation in 1-day-old hearts occurred independently of changes in 5'-AMP-activated protein kinase, acetyl-CoA carboxylase, or malonyl-CoA. The effect of gAd on fatty acid oxidation was reversed in the presence of 100 microunits/ml insulin. These results suggest that a decrease in plasma insulin and increase in gAd are involved in the increase of cardiac fatty acid oxidation in the immediate newborn period.
Highlights
Adiponectin is an adipocyte-derived polypeptide hormone of ϳ30-kDa [1]
We examined whether adiponectin or globular head domain (gAd) plays a role in this maturation of cardiac fatty acid oxidation
Because plasma insulin levels decrease and remain low throughout the suckling period, and because this decrease may contribute to the maturation of fatty acid oxidation, we examined the effects of adiponectin and gAd on fatty acid oxidation in isolated perfused 1-day-old rabbit hearts in the presence or absence of 100 microunits/ml insulin
Summary
Adiponectin is an adipocyte-derived polypeptide hormone of ϳ30-kDa [1]. It has a signal sequence at the N terminus, a small nonhelical region, a stretch of repeated collagens, and a C-terminal globular head domain (gAd) that makes up for the majority of the protein [2]. Stimulation of AMPK with full-length adiponectin reduces gluconeogenesis in the liver and plasma glucose [4] In agreement with these findings, Tomas et al [5] reported that gAd stimulates fatty acid oxidation in skeletal muscle by activating AMPK and inactivating ACC. The expression of AdipoR1 in C2C12 myocytes increased fatty acid oxidation and glucose uptake on stimulation with gAd, and these effects were partially inhibited by dominant negative AMPK. This suggests that AMPK is involved in the signaling through the adiponectin receptor. GAd, or control of AMPK by adiponectin and/or gAd contribute to the increase in fatty acid oxidation has not been determined
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