Endocrine responses of ovariectomized ewes to i.c.v. infusion of urocortin

Holmberg, B.J.; Morrison, C.D.; Keisler, D.H.

doi:10.1677/joe.0.1710517

Cited by 15 publications

(9 citation statements)

References 26 publications

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“…Effects on ACTH are most likely due to Ucn-1's CRF-like activity via pituitary CRF-R1s. This is in keeping with previous work showing Ucn-1-induced release of ACTH from isolated pituitary cells (1) and increased plasma ACTH and cortisol in animals (21,22,44).…”

Section: Discussionsupporting

confidence: 93%

Urocortin-1 Infusion in Normal Humans

Davis

Pemberton

Yandle

et al. 2004

The Journal of Clinical Endocrinology & Metabolism

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Urocortin-1 (Ucn-1), a member of the corticotropin-releasing factor family, has been shown in animal studies to have effects on the pituitary-adrenal axis, the cardiovascular system, circulating neurohormones, and renal function and to suppress appetite. For the first time in man we have evaluated these effects of infused Ucn-1 as well as actions on plasma ghrelin, a hormone known to increase appetite. We also assessed Ucn-1 pharmacokinetics. Eight healthy male volunteers consuming a diet of constant sodium and potassium content received 50 micro g Ucn-1 iv over 1 h in a placebo-controlled, randomized, time-matched, cross-over study. Ucn-1 infusion compared with placebo increased plasma levels of corticotropin [44.6 +/- 7.7 vs. 19.1 +/- 3.2 pg/ml (9.5 +/- 1.7 vs. 4.2 +/- 0.7 pmol/liter); P < 0.001], cortisol [15.6 +/- 1.6 vs. 7.7 +/- 1.4 micro g/dl (432 +/- 43 vs. 213 +/- 40 nmol/liter); P < 0.001], and atrial natriuretic peptide [26.2 +/- 3.4 vs. 21.3 +/- 2.2 pg/ml [8.5 +/- 1.1 vs. 6.9 +/- 0.7 pmol/liter); P = 0.019] while suppressing plasma ghrelin (P = 0.008). No hemodynamic or renal effects were observed at the dose used. The plasma Ucn-1 t(1/2) was 52 min based on a one-compartment model. In conclusion, a brief iv infusion of 50 micro g Ucn-1 stimulates plasma ACTH, cortisol, and atrial natriuretic peptide secretion and suppresses plasma ghrelin in healthy male volunteers. The latter effect might contribute to the anorexic action of Ucn-1.

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Section: Discussionsupporting

confidence: 93%

Urocortin-1 Infusion in Normal Humans

Davis

Pemberton

Yandle

et al. 2004

The Journal of Clinical Endocrinology & Metabolism

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“…While exogenous urocortin 1 administration can stimulate pituitary growth hormone release [39], the mechanism by which IGF-1 production is stimulated in Ucn3 + mice is more likely to be paracrine. Neither serum growth hormone nor hepatic IGF-1 levels were increased in Ucn3 + mice.…”

Section: Discussionmentioning

confidence: 99%

Urocortin 3 transgenic mice exhibit a metabolically favourable phenotype resisting obesity and hyperglycaemia on a high-fat diet

et al. 2011

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Aims/hypothesisUrocortins are the endogenous ligands for the corticotropin-releasing factor receptor type 2 (CRFR2), which is implicated in regulating energy balance and/or glucose metabolism. We determined the effects of chronic CRFR2 activation on metabolism in vivo, by generating and phenotyping transgenic mice overproducing the specific CRFR2 ligand urocortin 3.MethodsBody composition, glucose metabolism, insulin sensitivity, energy efficiency and expression of key metabolic genes were assessed in adult male urocortin 3 transgenic mice (Ucn3 +) under control conditions and following an obesogenic high-fat diet (HFD) challenge.ResultsUcn3+ mice had increased skeletal muscle mass with myocyte hypertrophy. Accelerated peripheral glucose disposal, increased respiratory exchange ratio and hypoglycaemia on fasting demonstrated increased carbohydrate metabolism. Insulin tolerance and indices of insulin-stimulated signalling were unchanged, indicating these effects were not mediated by increased insulin sensitivity. Expression of the transgene in Crfr2 (also known as Crhr2)-null mice negated key aspects of the Ucn3+ phenotype. Ucn3+ mice were protected from the HFD-induced hyperglycaemia and increased adiposity seen in control mice despite consuming more energy. Expression of uncoupling proteins 2 and 3 was higher in Ucn3+ muscle, suggesting increased catabolic processes. IGF-1 abundance was upregulated in Ucn3+ muscle, providing a potential paracrine mechanism in which urocortin 3 acts upon CRFR2 to link the altered metabolism and muscular hypertrophy observed.Conclusions/interpretationUrocortin 3 acting on CRFR2 in skeletal muscle of Ucn3 + mice results in a novel metabolically favourable phenotype, with lean body composition and protection against diet-induced obesity and hyperglycaemia. Urocortins and CRFR2 may be of interest as potential therapeutic targets for obesity.Electronic supplementary materialThe online version of this article (doi:10.1007/s00125-011-2205-6) contains supplementary material, which is available to authorised users.

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“…This action is likely via the CRH type 2 receptor, as urocortin, the endogenous ligand for the CRH type 2 receptor, stimulated LH concentrations and decreased feed intake in OVX ewes (Holmberg et al. ).…”

Section: Interaction Between Feeding and Reproduction Control By The Cnsmentioning

confidence: 99%

Hypothalamic Integration of Nutrient Status and Reproduction in the Sheep

Daniel

Foradori

Whitlock

et al. 2013

Reprod Domestic Animals

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Contents Nutrient availability is a determinant of reproductive success. It is well known that inadequate nutrition results in reproductive failure due to a number of factors including delay of puberty or anoestrous in post‐pubertal animals. The lack of nutrients is detected primarily by changes in circulating nutrient molecules and hormones and communicated directly or indirectly to the hypothalamus and brain stem for integration. The general effect is that low nutrition leads to increased appetite stimulation and reduced reproductive performance. When nutrition is adequate, the reverse is true. Both aspects will be the focus of this review. One result of the lack of nutrients is a reduction in luteinizing hormone (LH) concentrations and pulse frequency. Nutrient signals, such as glucose availability, hormonal signals, such as insulin and leptin, and neuroendocrine signals, such as neuropeptide Y and corticotropin‐releasing hormone, have been clearly demonstrated to interact to produce changes in LH and reproductive success. Other signals, such as fatty acids, ghrelin, agouti‐related peptide, melanin‐concentrating hormone, orexin, melanocyte‐stimulating hormone, kisspeptin, neurokinin, dynorphin and gonadotropin inhibitory hormone may also play a role in integrating nutrition and reproduction. This review will focus on the major features of the reciprocal control of appetite and reproduction in sheep.

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Endocrine responses of ovariectomized ewes to i.c.v. infusion of urocortin

Cited by 15 publications

References 26 publications

Urocortin-1 Infusion in Normal Humans

Urocortin-1 Infusion in Normal Humans

Urocortin 3 transgenic mice exhibit a metabolically favourable phenotype resisting obesity and hyperglycaemia on a high-fat diet

Hypothalamic Integration of Nutrient Status and Reproduction in the Sheep

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