C-Type Natriuretic Peptide as a New Regulator of Food Intake and Energy Expenditure

Inuzuka, Megumi; Tamura, Naohisa; Yamada, Nobuko; Katsuura, Goro; Oyamada, Naofumi; Taura, Daisuke; Sonoyama, Takuhiro; Fukunaga, Yasutomo; Ohinata, Kousaku; Sone, Masakatsu; Nakao, Kazuwa

doi:10.1210/jcem.95.7.9989

Cited by 7 publications

(9 citation statements)

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“…Guanylin and uroguanylin were identifi ed in the gastrointestinal tract as endogenous ligands for GC-C ( 11-16 ) and have since been thought to help maintain fl uid and salt homeostasis in a paracrine manner. GCs or their ligands, or both cascades, have recently been shown to contribute to energy metabolism ( 20,(35)(36)(37)(38). When fed an HFD, rats transgenic for BNP are protected from obesity and insulin resistance, and GC-A knockout mice have diet-induced obesity and glucose intolerance ( 20 ).…”

Section: Role Of Guanylin-gc-c System In Inhibition Of Droplet Formatmentioning

confidence: 99%

“…When fed an HFD, rats transgenic for BNP are protected from obesity and insulin resistance, and GC-A knockout mice have diet-induced obesity and glucose intolerance ( 20 ). In addition, CNP may play a role in regulating food intake and energy metabolism ( 35 ). However, the relationship between the guanylin-GC-C system and adipocyte regulation had not been investigated previously.…”

Section: Role Of Guanylin-gc-c System In Inhibition Of Droplet Formatmentioning

confidence: 99%

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Involvement of guanylin and GC-C in rat mesenteric macrophages in resistance to a high-fat diet

Akieda-Asai

Sugiyama

Miyazawa

et al. 2013

Journal of Lipid Research

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The worldwide incidence of obesity has accelerated during the last decade. Obesity is caused by excessive accumulation of white adipose tissue, often as the result of ingesting calories in excess of daily requirements ( 1, 2 ). In investigations of disease outcome, excess adipose tissue is defi ned by using the body mass index (BMI), which is calculated as weight (kg)/height (m 2 ). A BMI of 25.0-25.9 kg/m 2 corresponds to an overweight condition, whereas obesity is defi ned as a BMI of 30 kg/m 2 or greater ( 3, 4 ). Adipose depots in mammals are distributed throughout the body and include the fat surrounding the heart and the subcutaneous, retroperitoneal, and mesenteric fat. The amount of mesenteric fat is thought to be correlated most strongly with morbidity rate in obesity ( 5 ). Therefore, investigating the system regulating adipocytes in the mesenteric fat may yield insight into target molecules for treating or preventing obesity-related diseases.Both humans and animals vary in their body-weight responses to high-fat diets (HFDs). When animals are fed HFDs, most of them increase in body weight, with higher levels of adiposity than occur when standard chow is fed. However, a few subjects fed HFDs show less weight gain than do control animals fed standard chow or obesity-prone (diet-induced obesity, DIO) animals. These animals that do not become obese even when fed HFDs are categorized as being "diet resistant" (DR) ( 6, 7 ). To investigate the characteristics of genes expressed in the mesenteric fat tissues, we Abstract A high-fat diet (HFD) is a well-known contributing factor in the development of obesity. Most rats fed HFDs become obese. Those that avoid obesity when fed HFDs are considered diet resistant (DR). We performed a microarray screen to identify genes specifi c to the mesenteric fat of DR rats and revealed high expression of guanylin and guanylyl cyclase C (GC-C) in some subjects. Our histologic studies revealed that the cellular source of guanylin and GC-C is macrophages. Therefore, we developed double-transgenic (Tg) rats overexpressing guanylin and GC-C in macrophages and found that they were resistant to the effects of HFDs. In the mesenteric fat of HFD-fed Tg rats, Fas and perilipin mRNAs were downregulated, and those of genes involved in fatty acid oxidation were upregulated, compared with the levels in HFD-fed wild-type rats. In vitro studies demonstrated that lipid accumulation was markedly inhibited in adipocytes cocultured with macrophages expressing guanylin and GC-C and that this inhibition was reduced after treatment with guanylin-and GC-C-specifi c siRNAs. Our results suggest that the macrophagic guanylin-GC-C system contributes to the altered expression of genes involved in lipid metabolism, leading to resistance to obesity.

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Section: Role Of Guanylin-gc-c System In Inhibition Of Droplet Formatmentioning

confidence: 99%

Section: Role Of Guanylin-gc-c System In Inhibition Of Droplet Formatmentioning

confidence: 99%

Involvement of guanylin and GC-C in rat mesenteric macrophages in resistance to a high-fat diet

Akieda-Asai

Sugiyama

Miyazawa

et al. 2013

Journal of Lipid Research

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Section: Applications Of Serum Nt-procnp To Critical or Intensive Carementioning

confidence: 99%

“…Very recently, CNP has also been described as a regulator of glucose metabolism by acting as an inhibitor of insulin action (Inuzuka et al 2010). In a novel mouse model of inducible CNP depletion, CNP-deficient mice were found to have reduced food intake, lower endogenous insulin, and a significantly reduced insulin tolerance (Inuzuka et al 2010). Interestingly, NT-proCNP in critically ill patients was indeed correlated with endogenous insulin levels (C-peptide) as well as serum resistin and retinol-binding protein 4 (RBP4), two mediators of insulin resistance (data not shown) (Koch et al 2009(Koch et al , 2010.…”

Section: Applications Of Serum Nt-procnp To Critical or Intensive Carementioning

confidence: 99%

Critically Ill Patients and Circulating Amino-Terminal Pro-C-Type Natriuretic Peptide

Koch¹,

Tacke²

2014

Diet and Nutrition in Critical Care

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The natriuretic peptide family members, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP), exert multiple potent diuretic, natriuretic, and vasorelaxant functions, thereby directly influencing body-fluid homeostasis and blood pressure control. C-type natriuretic peptide (CNP) is mainly synthesized in the vasculature. We have evaluated the diagnostic and prognostic value of N-terminal proCNP (NT-proCNP) in 273 critically ill patients (197 patients with sepsis or septic shock, 76 without evidence of sepsis) in comparison to 43 healthy controls. Critically ill patients displayed significantly elevated NT-proCNP serum concentrations upon admission to the ICU compared to healthy controls, especially in conditions of sepsis. NT-proCNP correlated with inflammatory parameters (i.e., C-reactive protein, procalcitonin, and TNF-a), biomarkers of organ dysfunction, and clinical composite scores (APACHE II, SOFA, SAPS2). Despite its potential involvement in the pathogenesis of critical illness and sepsis, NT-proCNP may also be valuable as a prognostic biomarker in the ICU setting, because NT-proCNP levels at admission and day 3 were found to be predictive for ICU and overall survival. Further studies are warranted to elucidate the underlying pathomechanisms of NT-proCNP in critical illness and to validate its potential as a biomarker at the ICU.

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“…CNP suppresses oxygen consumption in BAT in mice by attenuating the sympathetic nervous system activity, possibly under the control of the hypothalamus (427) . Furthermore, it has been shown that natriuretic peptides can promote muscle mitochondrial biogenesis and fat oxidation, preventing the development of obesity and insulin resistance in mice (428) .…”

Section: Atrial Natriuretic Peptidesmentioning

confidence: 99%

Peripheral signalling involved in energy homeostasis control

2012

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The alarming prevalence of obesity has led to a better understanding of the molecular mechanisms controlling energy homeostasis. Regulation of energy intake and expenditure is more complex than previously thought, being influenced by signals from many peripheral tissues. In this sense, a wide variety of peripheral signals derived from different organs contributes to the regulation of body weight and energy expenditure. Besides the well-known role of insulin and adipokines, such as leptin and adiponectin, in the regulation of energy homeostasis, signals from other tissues not previously thought to play a role in body weight regulation have emerged in recent years. The role of fibroblast growth factor 21 (FGF21), insulin-like growth factor 1 (IGF-I), and sex hormone-binding globulin (SHBG) produced by the liver in the regulation of body weight and insulin sensitivity has been recently described. Moreover, molecules expressed by skeletal muscle such as myostatin have also been involved in adipose tissue regulation. Better known is the involvement of ghrelin, cholecystokinin, glucagon-like peptide 1 (GLP-1) and PYY 3 -36 , produced by the gut, in energy homeostasis. Even the kidney, through the production of renin, appears to regulate body weight, with mice lacking this hormone exhibiting resistance to diet-induced obesity. In addition, the skeleton has recently emerged as an endocrine organ, with effects on body weight control and glucose homeostasis through the actions of bone-derived factors such as osteocalcin and osteopontin. The comprehension of these signals will help in a better understanding of the aetiopathology of obesity, contributing to the potential development of new therapeutic targets aimed at tackling excess body fat accumulation.

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C-Type Natriuretic Peptide as a New Regulator of Food Intake and Energy Expenditure

Cited by 7 publications

References 0 publications

Involvement of guanylin and GC-C in rat mesenteric macrophages in resistance to a high-fat diet

Involvement of guanylin and GC-C in rat mesenteric macrophages in resistance to a high-fat diet

Critically Ill Patients and Circulating Amino-Terminal Pro-C-Type Natriuretic Peptide

Peripheral signalling involved in energy homeostasis control

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