Key result
Natriuretic peptides and the cGMP signaling system promote muscle mitochondrial biogenesis and fat oxidation, conferring resistance to diet-induced obesity and insulin resistance in mouse models.
Highlights new evidence that natriuretic peptides are involved in energy homeostasis and protection against high-fat diet effects.
In this issue of Diabetes, Miyashita et al. (1) providecompelling new evidence that natriuretic peptides(NPs) play a key role in the regulation of bodyweight and energy metabolism. In a series of com-plementary experiments, the investigators show that the NP–cyclic guanosine monophosphate (cGMP) signaling system increases the capacity for fat oxidation, activates mitochondrial biogenesis, and prevents the deleterious effects of a high-fat diet (HFD). NPs are not new players in metabolic regulation. Since the discovery of atrial natriuretic peptide (ANP) in 1980 (2), a large body of work has highlighted the multifaceted roles of NPs in the regulation of blood volume and arterial pressure. NPs are members of a family of structurally similar but genetically distinct endogenous peptide hor-mones. The NP family consists of at least three mamma-lian peptides: atrial-, brain-, and C-type (ANP, BNP, and CNP, respectively) (3). ANP and BNP preferentially bind
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Moro et al. (2009) conducted an editorial in Obesity and Type 2 Diabetes. Natriuretic peptides (NP-cGMP signaling) was evaluated. Natriuretic peptides and the cGMP signaling system promote muscle mitochondrial biogenesis and fat oxidation, conferring resistance to diet-induced obesity and insulin resistance in mouse models.
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