Impact of uraemia on food efficiency and the pulsatile mode of growth hormone secretion in rats

Krieg, Richard J.; Latta, Kay; Niimi, Kazuhiko; Veldhuis, Johannes D.; Chan, James C.M.

doi:10.1677/joe.0.1460509

Cited by 16 publications

(22 citation statements)

References 11 publications

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“…To measure the metabolic and leptin responses to the intravenous infusion of glucose, mannitol, galactose, or sodium chloride (NaCl), animals were anesthetized with isoflurane, and a catheter was inserted into the external jugular vein, as previously described (11). The infusion cannulas were tunneled subcutaneously to the back of the neck.…”

Section: Animals and Dietsmentioning

confidence: 99%

Plasma hyperosmolality stimulates leptin secretion acutely by a vasopressin-adrenal mechanism

Levy¹,

Stevens²

2004

American Journal of Physiology-Endocrinology and Metabolism

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Levy, James R., and Wayne Stevens. Plasma hyperosmolality stimulates leptin secretion acutely by a vasopressin-adrenal mechanism. Am J Physiol Endocrinol Metab 287: E263-E268, 2004. First published April 6, 2004; 10.1152/ajpendo.00514.2003.-Glucose administration to rodents acutely stimulates leptin secretion. To investigate the mechanism, rats were infused intravenously with various concentrations of glucose, and plasma leptin concentrations were measured with time. The osmolality of the infusates was equalized with various concentrations of carbohydrates that are not metabolized. Hyperosmolar glucose stimulates leptin secretion in a dose-dependent manner, with peak plasma leptin concentrations occurring ϳ3 h after the end of the glucose infusion. Hypertonic infusions of galactose, mannitol, and sodium chloride independently stimulate leptin secretion with approximately one-half the strength of equivalent osmolar concentrations of glucose. Peak plasma leptin concentrations occur ϳ4 h after the end of the hypertonic solution infusion. Hypertonic solutions of mannitol do not stimulate leptin secretion in vasopressindeficient or in adrenalectomized animals. In conclusion, intravenous infusions of hypertonic glucose and hypertonic mannitol independently stimulate leptin secretion. Hyperosmolality stimulates leptin secretion by a vasopressin-adrenal mechanism.LEPTIN IS A HORMONE SECRETED by adipocytes that has pleiotropic functions, including roles in body weight homeostasis, satiety, metabolism, reproduction, and angiogenesis (for review, see Ref. 1). The mechanisms of leptin secretion from adipocytes have been intensively studied. A number of factors, hormones, and conditions regulate leptin secretion. Fasting plasma leptin concentrations are mostly determined by body fat content; numerous investigations have demonstrated that both leptin mRNA and plasma leptin concentrations obtained from animals and humans after an overnight fast are directly proportional to measurements of body fat (6,18,19,27). In addition, leptin secretion is regulated by body fat-independent mechanisms. In rodents and humans, plasma leptin concentration has a diurnal variation that most likely is entrained to meals (4, 23). In the rodent, enteral feeding (26) or the intravenous infusion of total parenteral nutrition or glucose alone (15, 16) causes a rise in plasma leptin concentration ϳ3 h after the calorie bolus. The rise in insulin and the transport and metabolism of energyproducing substrates in adipocytes appear to stimulate postprandial leptin secretion (17,20).We previously showed that leptin secretion from cultured adipocytes was proportional to the uptake and metabolism of glucose and to the intra-adipocyte concentrations of ATP (14). We wanted to determine whether the previous studies in cultured adipocytes could be extended to studies in whole animals. We hypothesized that the intravenous infusion of increasing concentrations of glucose would increase delivery and metabolism of glucose in adipose tissue and acutely increase leptin...

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Section: Animals and Dietsmentioning

confidence: 99%

Plasma hyperosmolality stimulates leptin secretion acutely by a vasopressin-adrenal mechanism

Levy¹,

Stevens²

2004

American Journal of Physiology-Endocrinology and Metabolism

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“…Seventy-and 130-day old SD and F344 animals were anesthetized with isoflurane, and a catheter was inserted in the external jugular vein, as previously described (11). The infusion cannulas were tunneled subcutaneously to the back of the neck.…”

Section: Animals and Dietsmentioning

confidence: 99%

Lipid metabolism and resistin gene expression in insulin-resistant Fischer 344 rats

Levy

Davenport

Clore

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

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. Lipid metabolism and resistin gene expression in insulin-resistant Fischer 344 rats. Am J Physiol Endocrinol Metab 282: E626-E633, 2002; 10.1152/ajpendo. 00346.2001The interrelationship between insulin and leptin resistance in young Fischer 344 (F344) rats was studied. Young F344 and Sprague-Dawley (SD) rats were fed regular chow. F344 animals had two-to threefold higher insulin and triglyceride concentrations and increased stores of triglycerides within liver and muscle. F344 animals gained more body fat. Both acyl-CoA oxidase (ACO) and carnitine palmitoyltransferase I gene expression were 20-50% less in F344 animals than in age-matched SD animals. Peroxisome proliferator-activated receptor-␣ gene expression was reduced in 70-day-old F344 animals. Finally, resistin gene expression was similar in 70-day-old SD and F344 animals. Resistin gene expression increased fivefold in F344 animals and twofold in SD animals from 70 to 130 days, without a change in insulin sensitivity. We conclude that young F344 animals have both insulin and leptin resistance, which may lead to diminished fatty oxidation and accumulation of triglycerides in insulin-sensitive target tissues. We did not detect a role for resistin in the etiology of insulin resistance in F344 animals.Fischer 344 rats; acyl-coenzyme A oxidase; carnitine palmitoyltransferase I; peroxisome proliferator-activated receptor-␣

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“…Growth failure in uremia is well established in humans [1,2,3] and research animals [4]. Underlying mechanisms include possible decreases in the sensitivity of target tissues to growth hormone (GH) [5], as well as probable disruption of GH pulsatility [4].…”

Section: Introductionmentioning

confidence: 99%

Growth hormone and growth hormone-related mRNA in uremic rats: effect of a growth hormone secretagogue

et al. 2002

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In experimental animals, the decreased growth during mild uremia is not accompanied by a loss in the capacity of the pituitary gland to secrete growth hormone (GH). With the development of orally administered GH "secretagogues" (GHS), it might be possible to stimulate growth during uremia without injections. This study was designed to determine the effects of the GHS, L-163,255. Uremia was induced by 5/6 nephrectomy (NX). GHS was given orally, 3 mg/kg, twice a week. Four groups of animals included: (1) sham-operated, (2) sham-operated, pair-fed, (3) uremic (NX), and (4) uremic, GHS-treated (NX+GHS). Blood sampling was conducted via intra-atrial catheters, and GH was quantitated. Pituitary GH mRNA was measured by Northern blot, and liver GH receptor and insulin-like growth factor-I mRNAs by RNAase protection. Untreated NX animals had a specific decrease in the "mass" of the GH pulses. A burst of GH was induced by GHS, but the pulsatile pattern of GH secretion over 6 h was not affected. An increase or a return to non-uremic levels of GH-related mRNAs occurred after GHS. Thus, GHS stimulated an acute burst of GH secretion and increased specific mRNAs encoding GH-related proteins in uremic animals.

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Impact of uraemia on food efficiency and the pulsatile mode of growth hormone secretion in rats

Cited by 16 publications

References 11 publications

Plasma hyperosmolality stimulates leptin secretion acutely by a vasopressin-adrenal mechanism

Plasma hyperosmolality stimulates leptin secretion acutely by a vasopressin-adrenal mechanism

Lipid metabolism and resistin gene expression in insulin-resistant Fischer 344 rats

Growth hormone and growth hormone-related mRNA in uremic rats: effect of a growth hormone secretagogue

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