METABOLIC EFFECTS OF HYPERPHAGIA IN THE HYPOTHALAMIC-HYPERPHAGIC RAT

1966 ◽  
Vol 44 (4) ◽  
pp. 641-650 ◽  
Author(s):  
K. K. May ◽  
J. R. Beaton
Keyword(s):  
Spontaneous Activity ◽  
Body Weight Gain ◽  
Costal Cartilage ◽  
Metabolic Effects ◽  
Male Rats ◽  
Dynamic Phase ◽  
Static Phase ◽  
Electrolytic Lesions ◽  
Altered Thyroid

Metabolic effects of hyperphagia have been investigated in male rats in which hyperphagia was induced by bilateral, electrolytic lesions in the region of the ventromedial nuclei of the hypothalamus. In the early dynamic phase of hyperphagia, it would appear that increased body weight gain is a direct effect of increased energy intake not balanced by the observed increased spontaneous activity. In these animals increased lipogenesis (14C-acetate and 14C-glucose) and decreased lipolysis in vitro were evident with no evidence of altered thyroid function. Further, as determined by 35S incorporation in costal cartilage, the hyperphagia did not elicit an increased rate of skeletal growth. In the static phase, spontaneous activity was not increased, metabolic patterns were significantly altered in the direction of increased lipogenesis and decreased lipolysis, and there appeared to be a decreased uptake and release of 131I by the thyroid, which is suggestive of thyroid hypofunction.

scholarly journals In vitro pituitary and testicular effects of the leptin-related synthetic peptide leptin(116-130) amide involve actions both similar to and distinct from those of the native leptin molecule in the adult rat

2000 ◽  
pp. 406-410 ◽  
Author(s):  
M Tena-Sempere ◽  
L Pinilla ◽  
LC Gonzalez ◽  
J Navarro ◽  
C Dieguez ◽  
...  
Keyword(s):  
Body Weight ◽  
Adult Male ◽  
Body Weight Gain ◽  
Biologically Active ◽  
Male Rats ◽  
Male Rat ◽  
Gh Secretion ◽  
Adult Rat ◽  
Testosterone Secretion

The obese gene (ob) product, leptin, has recently emerged as a key element in body weight homeostasis, neuroendocrine function and fertility. Identification of biologically active, readily synthesized fragments of the leptin molecule has drawn considerable attention, as they may provide a powerful tool for detailed characterization of the biological actions of leptin in different experimental settings. Recently, a fragment of mouse leptin protein comprising amino acids 116-130, termed leptin(116-130) amide, was shown to mimic the effects of the native molecule in terms of body weight gain and food intake, and to elicit LH and prolactin (PRL) secretion in vivo. As a continuation of our previous experimental work, the present study reports on the effects of leptin(116-130) amide on basal and stimulated testosterone secretion by adult rat testis in vitro. In addition, a comparison of the effects of human recombinant leptin and leptin(116-130) amide at the pituitary level on the patterns of LH, FSH, PRL and GH secretion is presented. As reported previously by our group, human recombinant leptin(10(-9)-10(-7)M) significantly inhibited both basal and human chorionic gonadotrophin (hCG)-stimulated testosterone secretion in vitro. Similarly, incubation of testicular tissue in the presence of increasing concentrations of leptin(116-130) amide (10(-9)-10(-5)M) resulted in a dose-dependent inhibition of basal and hCG-stimulated testosterone secretion; a reduction that was significant from a dose of 10(-7)M upwards. In addition, leptin(116-130) amide, at all doses tested (10(-9)-10(-5)M), significantly decreased LH and FSH secretion by incubated hemi-pituitaries from adult male rats. In contrast, in the same experimental protocol, recombinant leptin(10(-9)-10(-7)M) was ineffective in modulating LH and FSH release. Finally, neither recombinant leptin nor leptin(116-130) amide were able to change basal PRL and GH secretion in vitro. Our results confirm the ability of leptin, acting at the testicular level, to inhibit testosterone secretion, and map the effect to a domain of the leptin molecule that lies between amino acid residues 116 and 130. In addition, we provide evidence for a direct inhibitory action of leptin(116-130) amide on pituitary LH and FSH secretion, a phenomenon not observed for the native leptin molecule, in the adult male rat.

MEAL-EATING AND LIPOGENESIS IN VITRO OF RATS FED A LOW-PROTEIN DIET

1964 ◽  
Vol 42 (5) ◽  
pp. 665-670 ◽  
Author(s):  
J. R. Beaton ◽  
V. Feleki ◽  
A. J. Szlavko ◽  
J. A. F. Stevenson
Keyword(s):  
Adipose Tissue ◽  
Food Intake ◽  
Body Weight Gain ◽  
Liver Glycogen ◽  
Male Rats ◽  
Acetate Incorporation ◽  
Casein Diet ◽  
Low Protein ◽  
Daily Food

The response of male rats to the restriction of food intake to 2 hours each day for 14 to 16 days has been assessed by the measurement of food intakes, body weights, liver glycogen concentrations, and lipogenesis of adipose tissue (C14-acetate incorporation in vitro). The animals were fed either a 20% casein diet (controls) or an isocaloric 5% casein diet. As a consequence of meal-eating, and regardless of dietary protein level, the average daily food intake and body weight gain were decreased whereas the lipogenesis in vitro and liver glycogen concentration were increased in comparison with rats fed ad libitum,which is in agreement with earlier findings using normal diets. These observations suggest that the decreased body fat of rats fed a 5% casein diet is not a consequence of an impaired ability of adipose tissue to synthesize fat.

PYY(3–36) reduces food intake and body weight and improves insulin sensitivity in rodent models of diet-induced obesity

2006 ◽  
Vol 291 (2) ◽  
pp. R367-R375 ◽  
Author(s):  
Niels Vrang ◽  
Andreas Nygaard Madsen ◽  
Mads Tang-Christensen ◽  
Gitte Hansen ◽  
Philip Just Larsen
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Peptide Yy ◽  
Body Weight Gain ◽  
Subcutaneous Administration ◽  
Treated Group ◽  
Metabolic Effects ◽  
Male Rats ◽  
Reduced Body ◽  
Gut Hormone

The gut hormone peptide YY (PYY) was recently proposed to comprise an endogenous satiety factor. We have studied acute anorectic functions of PYY(3–36) in mice and rats, as well as metabolic effects of chronic PYY(3–36) administration to diet-induced obese (DIO) mice and rats. A single intraperitoneal injection of PYY(3–36) inhibited food intake in mice, but not in rats. We next investigated the effects of increasing doses (100, 300, and 1,000 μg·kg−1·day−1) of PYY(3–36) administered subcutaneously via osmotic minipumps on food intake and body weight in DIO C57BL/6J mice. Whereas only the highest dose (1,000 μg·kg−1·day−1) of PYY(3–36) significantly reduced food intake over the first 3 days, body weight gain was dose dependently reduced, and on day 28 the group treated with 1,000 μg·kg−1·day−1 PYY(3–36) weighed ∼10% less than the vehicle-treated group. Mesenteric, epididymal, retroperitoneal, and inguinal fat pad weight was dose dependently reduced. Subcutaneous administration of PYY(3–36) (250 and 1,000 μg·kg−1·day−1) for 28 days reduced body weight and improved glycemic control in glucose-intolerant DIO rats. Neither 250 nor 1,000 μg/kg PYY(3–36) elicited a conditioned taste aversion in male rats.

scholarly journals METABOLIC EFFECTS OF LATHYROGENIC AGENTS ON CARTILAGE IN VIVO AND IN VITRO

1961 ◽  
Vol 113 (2) ◽  
pp. 381-403 ◽  
Author(s):  
Morris J. Karnovsky ◽  
Manfred L. Karnovsky
Keyword(s):  
Chondroitin Sulfate ◽  
Costal Cartilage ◽  
Epiphyseal Cartilage ◽  
Metabolic Effects ◽  
In Vitro System ◽  
Low Concentrations ◽  
Biochemical Indices ◽  
Hexosamine Content

The effects of lathyrogenic agents in vivo and in vitro are described, in respect to some biochemical indices of cartilage metabolism. Lathyrogenic agents in vivo inhibited the incorporation of radiosulfate into rat epiphyseal cartilage and the isolated chondroitin sulfate. No significant changes in hydroxyproline or hexosamine content of epiphyseal cartilage were found, but there was a marked increase in water content. The content of chondroitin sulfate, measured as uronic acid, was decreased. The importance of taking growth rate differences between control and experimental rats into account in assessing the effects of lathyrogenic agents in vivo is emphasized. In an in vitro system, utilizing fresh calf costal cartilage slices, the presence of low concentrations of lathyrogenic agents markedly affected various metabolic events. The incorporation into cartilage slices of sulfate-S35, glucose-U-C14, and glycine-1-C14 was significantly depressed, as was the production of organic acids, including lactic acid. In general, these effects were more severe under anaerobic conditions. Glutamine restored the activities of the slices treated with lathyrogenic agents to control values obtained in the absence of either lathyrogen or glutamine.

Metabolic effects of chronic infusions of epinephrine and norepinephrine in rats

1986 ◽  
Vol 250 (5) ◽  
pp. E518-E522 ◽  
Author(s):  
R. Racotta ◽  
L. Ramirez-Altamirano ◽  
E. Velasco-Delgado
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Body Weight Gain ◽  
Serum Insulin ◽  
Chronic Administration ◽  
Metabolic Effects ◽  
Male Rats ◽  
Epinephrine Infusion ◽  
Calculated Dose

Chronic infusions of epinephrine, norepinephrine, or vehicle were performed in adult male rats by means of subcutaneous implanted osmotic minipumps (ALZET). The calculated dose was 180 ng/min during 7-8 days. Daily food intake and body weight were measured during this period and also 7 days before and 5 days after it. During the period of infusion, norepinephrine stopped body weight gain while epinephrine-infused rats gained weight at the same rate as controls. Once the infusion period was finished, epinephrine-infused rats gained more weight than controls, while norepinephrine-infused rats just returned to the slope of weight gain of the controls. In no group did food intake change. In a second experiment, similar infusions were carried out in other rats on the same schedule; body temperature, glycemia, and serum insulin and triiodothyronine were measured. Epinephrine infusion significantly elevated glycemia and triiodothyronine, whereas norepinephrine infusion increased temperature and serum insulin. The results obtained by chronic administration of the catecholamines support the concept of a disassociation of adrenomedullary and sympathetic nervous system metabolic effects.

Dynamic and static phases of obesity following lesions in PVN and VMH

1987 ◽  
Vol 253 (3) ◽  
pp. R523-R529 ◽  
Author(s):  
M. Fukushima ◽  
K. Tokunaga ◽  
J. Lupien ◽  
J. W. Kemnitz ◽  
G. A. Bray
Keyword(s):  
Weight Gain ◽  
Food Intake ◽  
Ventromedial Hypothalamus ◽  
Similar Degree ◽  
Rapid Weight Gain ◽  
Interscapular Brown Adipose Tissue ◽  
Dynamic Phase ◽  
Brown Adipose ◽  
Static Phase ◽  
Electrolytic Lesions

The effect of electrolytic lesions in the ventromedial hypothalamus (VMH) and the paraventricular nucleus (PVN) has been compared during both the dynamic and static phase of weight gain. Hyperphagia and weight gain were greater in the VMH-lesioned rats than in the PVN-lesioned rats. Food intake increased at night after both lesions but increased in the daytime only in VMH-lesioned rats. During the dynamic phase of rapid weight gain, the diurnal pattern of corticosterone was blunted to a similar degree in both lesioned groups. The morning insulin concentrations were higher in both lesioned groups than in the sham-operated controls, but in the static phase only the VMH-lesioned rats had higher insulin levels. In the afternoon the insulin was higher in the VMH-lesioned rats than in either the sham-operated or PVN-lesioned rats. In the dynamic phase the weight of interscapular brown adipose tissue was significantly increased in the VMH-lesioned rats, but the specific GDP binding was depressed both in the morning and afternoon when compared with either the sham-operated or PVN-lesioned groups. In both the dynamic and static phases GDP binding was similar in sham-operated and PVN-lesioned animals. The differences in concentration of corticosterone in morning and afternoon were smaller in the lesioned groups than in the controls. These data are consistent with the hypothesis that animals with PVN lesions do not show the disturbances in food intake or in the autonomic nervous system that characterize the VMH-lesioned rats.

scholarly journals Castration differentially alters basal and leucine-stimulated tissue protein synthesis in skeletal muscle and adipose tissue

2009 ◽  
Vol 297 (5) ◽  
pp. E1222-E1232 ◽  
Author(s):  
Qianning Jiao ◽  
Anne M. Pruznak ◽  
Danuta Huber ◽  
Thomas C. Vary ◽  
Charles H. Lang
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Adipose Tissue ◽  
Muscle Protein ◽  
Body Weight Gain ◽  
Muscle Protein Synthesis ◽  
Male Rats ◽  
Whole Body ◽  
Fat Depot

Reduced testosterone as a result of catabolic illness or aging is associated with loss of muscle and increased adiposity. We hypothesized that these changes in body composition occur because of altered rates of protein synthesis under basal and nutrient-stimulated conditions that are tissue specific. The present study investigated such mechanisms in castrated male rats (75% reduction in testosterone) with demonstrated glucose intolerance. Over 9 wk, castration impaired body weight gain, which resulted from a reduced lean body mass and preferential sparing of adipose tissue. Castration decreased gastrocnemius weight, but this atrophy was not associated with reduced basal muscle protein synthesis or differences in plasma IGF-I, insulin, or individual amino acids. However, oral leucine failed to normally stimulate muscle protein synthesis in castrated rats. In addition, castration-induced atrophy was associated with increased 3-methylhistidine excretion and in vitro-determined ubiquitin proteasome activity in skeletal muscle, changes that were associated with decreased atrogin-1 or MuRF1 mRNA expression. Castration decreased heart and kidney weight without reducing protein synthesis and did not alter either cardiac output or glomerular filtration. In contradistinction, the weight of the retroperitoneal fat depot was increased in castrated rats. This increase was associated with an elevated rate of basal protein synthesis, which was unresponsive to leucine stimulation. Castration also decreased whole body fat oxidation. Castration increased TNFα, IL-1α, IL-6, and NOS2 mRNA in fat but not muscle. In summary, the castration-induced muscle wasting results from an increased muscle protein breakdown and the inability of leucine to stimulate protein synthesis, whereas the expansion of the retroperitoneal fat depot appears mediated in part by an increased basal rate of protein synthesis-associated increased inflammatory cytokine expression.

The interrelationships of thyroid and growth hormones: effect of growth hormone releasing hormone in hypo- and hyperthyroid male rats

1986 ◽  
Vol 113 (4_Suppl) ◽  
pp. S367-S375 ◽  
Author(s):  
Allen W. ROOT ◽  
Dorothy SHULMAN ◽  
Jennifer ROOT ◽  
Frank DIAMOND
Keyword(s):  
Growth Hormone ◽  
Thyroid Hormones ◽  
Secretory Response ◽  
Metabolic Effects ◽  
Male Rats ◽  
Male Rat ◽  
Peripheral Tissues ◽  
Releasing Hormone

ABSTRACT Growth hormone (GH) and the thyroid hormones interact in the hypothalamus, pituitary and peripheral tissues. Thyroid hormone exerts a permissive effect upon the anabolic and metabolic effects of GH, and increases pituitary synthesis of this protein hormone. GH depresses the secretion of thyrotropin and the thyroid hormones and increases the peripheral conversion of thyroxine to triiodothyronine. In the adult male rat experimental hypothyroidism produced by ingestion of propylthiouracil depresses the GH secretory response to GH-releasing hormone in vivo and in vitro, reflecting the lowered pituitary stores of GH in the hypothyroid state. Short term administration of large amounts of thyroxine with induction of the hyperthyroid state does not affect the in vivo GH secretory response to GH-releasing hormone in this animal.

scholarly journals Behavioral and Metabolic Effects of a Calorie-Restricted Cafeteria Diet and Oleuropein Supplementation in Obese Male Rats

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4474
Author(s):  
Alex Subias-Gusils ◽  
Adam Álvarez-Monell ◽  
Noemí Boqué ◽  
Antoni Caimari ◽  
Josep M. Del Bas ◽  
...  
Keyword(s):  
Body Weight ◽  
Dietary Intervention ◽  
Body Weight Gain ◽  
High Energy ◽  
Sweet Taste ◽  
Cafeteria Diet ◽  
Metabolic Effects ◽  
Male Rats ◽  
Sucrose Intake ◽  
Obese Rats

Diet-induced obesity models are widely used to investigate dietary interventions for treating obesity. This study was aimed to test whether a dietary intervention based on a calorie-restricted cafeteria diet (CAF-R) and a polyphenolic compound (Oleuropein, OLE) supplementation modified sucrose intake, preference, and taste reactivity in cafeteria diet (CAF)-induced obese rats. CAF diet consists of high-energy, highly palatable human foods. Male rats fed standard chow (STD) or CAF diet were compared with obese rats fed CAF-R diet, alone or supplemented with an olive tree leaves extract (25 mg/kg*day) containing a 20.1% of OLE (CAF-RO). Biometric, food consumption, and serum parameters were measured. CAF diet increased body weight, food and energy consumption and obesity-associated metabolic parameters. CAF-R and CAF-RO diets significantly attenuated body weight gain and BMI, diminished food and energy intake and improved biochemical parameters such as triacylglycerides and insulin resistance which did not differ between CAF-RO and STD groups. The three cafeteria groups diminished sucrose intake and preference compared to STD group. CAF-RO also diminished the hedonic responses for the high sucrose concentrations compared with the other groups. These results indicate that CAF-R diet may be an efficient strategy to restore obesity-associated alterations, whilst OLE supplementation seems to have an additional beneficial effect on sweet taste function.

Fine Structural Changes in the Adenohypophyses of Rats Following Destruction of the Pituitary Stalk

1977 ◽  
Vol 35 ◽  
pp. 496-497
Author(s):  
K. Kovacs ◽  
E. Horvath ◽  
J. M. Bilbao ◽  
F. A. Laszlo ◽  
I. Domokos
Keyword(s):  
Structural Changes ◽  
Tissue Injury ◽  
Anterior Lobe ◽  
Uranyl Acetate ◽  
Male Rats ◽  
Pituitary Stalk ◽  
Sequence Of Events ◽  
Pituitary Glands ◽  
Electrolytic Lesions ◽  
Ultrathin Sections

Electrolytic lesions of the pituitary stalk in rats interrupt adenohypophysial blood flow and result in massive infarction of the anterior lobe. In order to obtain a deeper insight into the morphogenesis of tissue injury and to reveal the sequence of events, a fine structural investigation was undertaken on adenohypophyses of rats at various intervals following destruction of the pituitary stalk.The pituitary stalk was destroyed electrolytically, with a Horsley-Clarke apparatus on 27 male rats of the R-Amsterdam strain, weighing 180-200 g. Thirty minutes, 1,2,4,6 and 24 hours after surgery the animals were perfused with a glutaraldehyde-formalin solution. The skulls were then opened and the pituitary glands removed. The anterior lobes were fixed in glutaraldehyde-formalin solution, postfixed in osmium tetroxide and embedded in Durcupan. Ultrathin sections were stained with uranyl acetate and lead citrate and investigated with a Philips 300 electron microscope.

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