scholarly journals Effects of pair-feeding and growth hormone treatment on obese transgenic rats

2002 ◽  
pp. 245-249 ◽  
Author(s):  
Y Furuhata ◽  
K Hirabayashi ◽  
T Yonezawa ◽  
M Takahashi ◽  
M Nishihara
Keyword(s):  
Body Weight ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Food Intake ◽  
Caloric Intake ◽  
Serum Triglyceride ◽  
Metabolic Abnormalities ◽  
Transgenic Rats ◽  
Serum Free Fatty Acid ◽  
Fat Accumulation

BACKGROUND: It has been shown that GH-deficient subjects tend to have fat accumulation. We have produced human GH (hGH) transgenic rats that exhibit low circulating hGH levels and hyperphagia. These rats are also characterized by severe obesity, hyperinsulinemia and hyperlipidemia. OBJECTIVE: The present study was conducted in order to elucidate how excess caloric intake and impaired GH secretion account for fat accumulation and metabolic abnormalities in the transgenic rats. DESIGN AND METHODS: The transgenic rats were subjected to either pair-feeding with non-transgenic controls or hGH treatment from 4 to 12 weeks of age, and the effects on fat accumulation and some metabolic parameters were assessed. RESULTS: At the age of 12 weeks, body weight and food intake were greater in transgenic than in control rats by 10% and 27% respectively. The ratio of epididymal white adipose tissue weight to body weight (WAT/BW) was more than three times greater in transgenic than in control rats. Although pair-feeding for 8 weeks decreased body weight, it did not affect the WAT/BW ratio. Treatment with hGH affected neither body weight nor food intake, while it reduced the WAT/BW ratio by 30%. Serum concentrations of triglyceride, free fatty acid, insulin and leptin were all significantly higher in the transgenic than in the control rats. Pair-feeding decreased serum triglyceride, insulin and leptin levels, but not serum free fatty acid levels. On the other hand, hGH treatment decreased only serum leptin concentrations. CONCLUSIONS: These results suggest that severe fat accumulation in the transgenic rats mainly resulted from the decreased lipolytic action of GH, while metabolic abnormalities mainly resulted from excess caloric intake.

scholarly journals Dietary thylakoids reduce visceral fat mass and increase expression of genes involved in intestinal fatty acid oxidation in high-fat fed rats

2016 ◽  
Vol 311 (3) ◽  
pp. R618-R627 ◽  
Author(s):  
Eva-Lena Stenblom ◽  
Emil Egecioglu ◽  
Caroline Montelius ◽  
Deepti Ramachandran ◽  
Britta Bonn ◽  
...  
Keyword(s):  
Body Weight ◽  
Fatty Acid ◽  
Food Intake ◽  
Fatty Acid Oxidation ◽  
Body Fat ◽  
Dietary Fat ◽  
Visceral Fat ◽  
Acid Oxidation ◽  
High Fat ◽  
Fat Accumulation

Thylakoids reduce body weight gain and body fat accumulation in rodents. This study investigated whether an enhanced oxidation of dietary fat-derived fatty acids in the intestine contributes to the thylakoid effects. Male Sprague-Dawley rats were fed a high-fat diet with ( n = 8) or without thylakoids ( n = 8) for 2 wk. Body weight, food intake, and body fat were measured, and intestinal mucosa was collected and analyzed. Quantitative real-time PCR was used to measure gene expression levels of key enzymes involved in fatty acid transport, fatty acid oxidation, and ketogenesis. Another set of thylakoid-treated ( n = 10) and control rats ( n = 10) went through indirect calorimetry. In the first experiment, thylakoid-treated rats ( n = 8) accumulated 25% less visceral fat than controls. Furthermore, fatty acid translocase ( Fat/Cd36), carnitine palmitoyltransferase 1a ( Cpt1a), and mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase 2 ( Hmgcs2) genes were upregulated in the jejunum of the thylakoid-treated group. In the second experiment, thylakoid-treated rats ( n = 10) gained 17.5% less weight compared with controls and their respiratory quotient was lower, 0.86 compared with 0.91. Thylakoid-intake resulted in decreased food intake and did not cause steatorrhea. These results suggest that thylakoids stimulated intestinal fatty acid oxidation and ketogenesis, resulting in an increased ability of the intestine to handle dietary fat. The increased fatty acid oxidation and the resulting reduction in food intake may contribute to the reduced fat accumulation in thylakoid-treated animals.

Protein appetite is increased after central leptin-induced fat depletion

2007 ◽  
Vol 293 (4) ◽  
pp. R1468-R1473 ◽  
Author(s):  
Michael F. Wiater ◽  
Bryan D. Hudson ◽  
Yvette Virgin ◽  
Sue Ritter
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Body Fat ◽  
Caloric Intake ◽  
Sprague Dawley ◽  
Body Protein ◽  
Macronutrient Selection ◽  
Daily Diet ◽  
Nadir Point ◽  
And Control

Leptin reduces body fat selectively, sparing body protein. Accordingly, during chronic leptin administration, food intake is suppressed, and body weight is reduced until body fat is depleted. Body weight then stabilizes at this fat-depleted nadir, while food intake returns to normal caloric levels, presumably in defense of energy and nutritional homeostasis. This model of leptin treatment offers the opportunity to examine controls of food intake that are independent of leptin's actions, and provides a window for examining the nature of feeding controls in a “fatless” animal. Here we evaluate macronutrient selection during this fat-depleted phase of leptin treatment. Adult, male Sprague-Dawley rats were maintained on standard pelleted rodent chow and given daily lateral ventricular injections of leptin or vehicle solution until body weight reached the nadir point and food intake returned to normal levels. Injections were then continued for 8 days, during which rats self-selected their daily diet from separate sources of carbohydrate, protein, and fat. Macronutrient choice differed profoundly in leptin and control rats. Leptin rats exhibited a dramatic increase in protein intake, whereas controls exhibited a strong carbohydrate preference. Fat intake did not differ between groups at any time during the 8-day test. Despite these dramatic differences in macronutrient selection, total daily caloric intake did not differ between groups except on day 2. Thus controls of food intake related to ongoing metabolic and nutritional requirements may supersede the negative feedback signals related to body fat stores.

scholarly journals The long-chain fatty acid receptors FFA1 and FFA4 are involved in food intake regulation in fish brain

2020 ◽  
Vol 223 (17) ◽  
pp. jeb227330
Author(s):  
Cristina Velasco ◽  
Marta Conde-Sieira ◽  
Sara Comesaña ◽  
Mauro Chivite ◽  
Adrián Díaz-Rúa ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Food Intake ◽  
Mrna Abundance ◽  
Fish Brain ◽  
Protein Levels ◽  
Food Intake Regulation ◽  
Free Fatty Acid Receptors ◽  
Intake Regulation ◽  
Long Chain

ABSTRACTWe hypothesized that the free fatty acid receptors FFA1 and FFA4 might be involved in the anorectic response observed in fish after rising levels of long-chain fatty acids (LCFAs) such as oleate. In one experiment we demonstrated that intracerebroventricular (i.c.v.) treatment of rainbow trout with FFA1 and FFA4 agonists elicited an anorectic response 2, 6 and 24 h after treatment. In a second experiment, the same i.c.v. treatment resulted after 2 h in an enhancement in the mRNA abundance of anorexigenic neuropeptides pomca1 and cartpt and a decrease in the values of orexigenic peptides npy and agrp1. These changes occurred in parallel with those observed in the mRNA abundance and/or protein levels of the transcription factors Creb, Bsx and FoxO1, protein levels and phosphorylation status of Ampkα and Akt, and mRNA abundance of plcb1 and itrp3. Finally, we assessed in a third experiment the response of all these parameters after 2 h of i.c.v. treatment with oleate (the endogenous ligand of both free fatty acid receptors) alone or in the presence of FFA1 and FFA4 antagonists. Most effects of oleate disappeared in the presence of FFA1 and FFA4 antagonists. The evidence obtained supports the involvement of FFA1 and FFA4 in fatty acid sensing in fish brain, and thus involvement in food intake regulation through mechanisms not exactly comparable (differential response of neuropeptides and cellular signalling) to those known in mammals.

Elevated serum free fatty acid concentrations inhibit T lymphocyte signaling

2000 ◽  
Vol 14 (7) ◽  
pp. 939-947 ◽  
Author(s):  
Thomas M. Stulnig ◽  
Markus Berger ◽  
Michael Roden ◽  
Harald Stingl ◽  
Daniel Raederstorff ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
T Lymphocyte ◽  
Elevated Serum ◽  
Serum Free Fatty Acid ◽  
Serum Free

scholarly journals Association of Serum–Free Fatty Acid Level With Reduced Reflection Pressure Wave Magnitude and Central Blood Pressure

Hypertension ◽  
2014 ◽  
Vol 64 (6) ◽  
pp. 1212-1218 ◽  
Author(s):  
Yasuharu Tabara ◽  
Yoshimitsu Takahashi ◽  
Takahisa Kawaguchi ◽  
Kazuya Setoh ◽  
Chikashi Terao ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Pressure Wave ◽  
Acid Level ◽  
Free Fatty Acid Level ◽  
Central Blood Pressure ◽  
Fatty Acid Level ◽  
Serum Free Fatty Acid ◽  
Serum Free

scholarly journals Metabolic Effects of Catecholamines in Sheep

1970 ◽  
Vol 23 (4) ◽  
pp. 903 ◽  
Author(s):  
JM Bassett
Keyword(s):  
Body Weight ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Intravenous Injection ◽  
Intravenous Infusion ◽  
Plasma Insulin ◽  
Metabolic Effects ◽  
Plasma Insulin Concentration ◽  
Adrenaline Infusion ◽  
Adrenaline Injection

Intravenous infusion of 1� 5 mg adrenaline over 30 min into adult Merino wethers (50 kg body weight), increased glucose, lactate, and free fatty acid (FFA) concentrations in plasma much more than did a single rapid intravenous injection of the same amount. There was no increase in plasma insulin concentration during adrenaline infusion or after adrenaline injection.

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