Exercise-induced lipid mobilization in subcutaneous adipose tissue is mainly related to natriuretic peptides in overweight men

Moro, Cédric; Pillard, Fabien; Glisezinski, Isabelle de; Klimčáková, Eva; Crampes, F.; Thalamas, Claire; Harant, I.; Marqués, Marie-Adeline; Lafontan, Max; Berlan, Michel

doi:10.1152/ajpendo.90227.2008

Cited by 51 publications

(46 citation statements)

References 34 publications

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“…A physiological role for NPs in exercise-induced lipolysis in humans has been suggested (16)(17)(18). The increased cardiac output with exercise and release of NPs suggests that the heart has a central role in regulating the supply of fatty acids for both cardiac and skeletal muscle under aerobic conditions.…”

Section: Introductionmentioning

confidence: 99%

Cardiac natriuretic peptides act via p38 MAPK to induce the brown fat thermogenic program in mouse and human adipocytes

Bordicchia¹,

Liu²,

Amri³

et al. 2012

J. Clin. Invest.

770

559

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The ability of mammals to resist body fat accumulation is linked to their ability to expand the number and activity of "brown adipocytes" within white fat depots. Activation of β-adrenergic receptors (β-ARs) can induce a functional "brown-like" adipocyte phenotype. As cardiac natriuretic peptides (NPs) and β-AR agonists are similarly potent at stimulating lipolysis in human adipocytes, we investigated whether NPs could induce human and mouse adipocytes to acquire brown adipocyte features, including a capacity for thermogenic energy expenditure mediated by uncoupling protein 1 (UCP1). In human adipocytes, atrial NP (ANP) and ventricular NP (BNP) activated PPARγ coactivator-1α (PGC-1α) and UCP1 expression, induced mitochondriogenesis, and increased uncoupled and total respiration. At low concentrations, ANP and β-AR agonists additively enhanced expression of brown fat and mitochondrial markers in a p38 MAPK-dependent manner. Mice exposed to cold temperatures had increased levels of circulating NPs as well as higher expression of NP signaling receptor and lower expression of the NP clearance receptor (Nprc) in brown adipose tissue (BAT) and white adipose tissue (WAT). NPR-C -/-mice had markedly smaller WAT and BAT depots but higher expression of thermogenic genes such as Ucp1. Infusion of BNP into mice robustly increased Ucp1 and Pgc-1α expression in WAT and BAT, with corresponding elevation of respiration and energy expenditure. These results suggest that NPs promote "browning" of white adipocytes to increase energy expenditure, defining the heart as a central regulator of adipose tissue biology. IntroductionThe cardiac natriuretic peptides (NPs), atrial NP (ANP) and its ventricular companion (BNP), are key hormones in fluid and hemodynamic homeostasis. Their actions are mediated by binding to NP receptor A (NPRA), whose intracellular domain possesses guanylyl cyclase activity to generate the second messenger cGMP (1, 2). Another member of the NP receptor family (NPRC, which is referred to as the clearance receptor) also binds ANP and BNP to remove them from circulation (3). Almost 2 decades ago, NP receptors were unexpectedly found to be expressed in adipose tissue of both rats (4) and humans (5), and, interestingly, levels of NPRC in adipose tissue were found to be sharply decreased by fasting in rats (6). Together, these were some of the first results to suggest that perhaps cardiac NPs have a metabolic role in adipocytes, including a putative role for adipose tissue in the clearance of these peptides from the circulation (7).ANP was subsequently shown to increase lipolysis in human adipocytes, with a potency similar to that of catecholamines (8), which are the well-established physiological pathway controlling lipolysis through activation of the β-adrenergic receptors (β-ARs). Interestingly, the ability of NPs to stimulate lipolysis was reported to be primate specific and apparently absent from rodent adipose tissue (9). To understand this process mechanistically, recall that β-ARs, as the classic stimulator o...

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Section: Introductionmentioning

confidence: 99%

Cardiac natriuretic peptides act via p38 MAPK to induce the brown fat thermogenic program in mouse and human adipocytes

Bordicchia¹,

Liu²,

Amri³

et al. 2012

J. Clin. Invest.

770

559

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“…ANP is one of the two most important agents regulating lipolysis and ATBF during exercice (131,164). A negative correlation between ANP levels and BMI was found in obese people.…”

Section: Other Possible Causes Of Perturbed Atbfmentioning

confidence: 97%

Update on adipose tissue blood flow regulation

Sotorník

Brassard

Martin

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

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According to Fick's principle, any metabolic or hormonal exchange through a given tissue depends on the product of the blood flow to that tissue and the arteriovenous difference. The proper function of adipose tissue relies on adequate adipose tissue blood flow (ATBF), which determines the influx and efflux of metabolites as well as regulatory endocrine signals. Adequate functioning of adipose tissue in intermediary metabolism requires finely tuned perfusion. Because metabolic and vascular processes are so tightly interconnected, any disruption in one will necessarily impact the other. Although altered ATBF is one consequence of expanding fat tissue, it may also aggravate the negative impacts of obesity on the body's metabolic milieu. This review attempts to summarize the current state of knowledge on adipose tissue vascular bed behavior under physiological conditions and the various factors that contribute to its regulation as well as the possible participation of altered ATBF in the pathophysiology of metabolic syndrome. obesity; insulin; sympathetic nervous system; nitric oxide; angiotensin II; atrial natriuretic peptide; glucagon-like peptide-1; glucose-dependent insulinotropic polypeptide OVER THE LAST DECADES, THE WORLDWIDE PANDEMIC of obesity, metabolic syndrome, and type 2 diabetes mellitus (T2DM) (188) has attracted ever-increasing attention to the role and significance of adipose tissue (AT). Originally regarded as a mere energy store with insulation and protective cushioning functions, AT is now recognized as a bona fide and highly active metabolic and endocrine organ (102). It has also become evident that the white AT is a heterogeneous tissue. From a metabolic point of view, AT can be subdivided into central (abdominal) and peripheral (hips and buttocks) depots (78). Although extra-abdominal fat accumulation does not bring upon higher metabolic and cardiovascular risk, some reports show a protective influence (124). Conversely, a negative metabolic effect has been associated with central fat (102), which in fact comprises two distinct masses (visceral and subcutaneous) with different metabolic and hormonal activities and impacts on metabolic syndrome pathogenesis (95) and blood flow rates (102).Metabolic processes in fatty tissue require adequate substrate(s) and humoral factor delivery (76). Conversely, adipocytes communicate with other metabolically active tissues through humoral factors (128) as well as through metabolic products (118) serving as energetic substrates. Humoral factors derived from AT arise not only from adipocytes themselves but also from other components of AT such as macrophages and endothelial cells. Moreover, AT is a known conversion site for several hormones or humoral factors, e.g., steroid hormones (156) or components of the renin-angiotensin-aldosterone system (RAAS). All of these functions of AT are tightly linked to the pattern of blood supply and its regulation, which largely differ from other metabolically active organs such as the liver or skeletal muscle (141).In add...

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“…However, work published by Moro et al 10 adds insight to this problem. These researchers found that lipid mobilization in subcutaneous adipose tissue due to physical exercise observed in overweight patients was associated with a rise in plasma levels of atrial NP.…”

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confidence: 99%