Effect of Genetic Obesity on Thermoregulatory Activity Responses to Inversion of the Light/Dark Cycle

2001 ◽  
Vol 2 (4) ◽  
pp. 249-256 ◽  
Author(s):  
Patricia A. Jarosz ◽  
Terry A. Lennie ◽  
Pamela J. Rowsey ◽  
Bonnie L. Metzger
Keyword(s):  
Total Activity ◽  
Zucker Rats ◽  
Sprague Dawley ◽  
Genetic Obesity ◽  
Temperature Rhythm ◽  
Sprague Dawley Rats ◽  
Pilot Work ◽  
Obese Zucker Rats ◽  
Reversal Temperature ◽  
Fatty Zucker Rat

In this pilot work, the authors compared the circadian rhythm responses of 3-month-old female fatty Zucker rats with those of lean Zucker rats and Sprague-Dawley rats to reversal of the light/dark (LD) cycle. Core temperature and spontaneous cage activity were continuously monitored by implanted microtelemetry devices prior to and for 5 days following complete LD cycle reversal. By the 5th day after LD reversal, temperature rhythm nadir had phase-advanced 10.5 hours in the lean Zucker rats, 10.8 hours in the Sprague-Dawley rats, and only 3.8 hours in the fatty Zucker rats. Similarly, total activity increased in lean Zucker rats and Sprague-Dawley rats after LD reversal but declined in the fatty Zucker rat during the same time. Results of this study show that obese Zucker rats displayed an impaired ability to reentrain circadian rhythms for temperature and activity when compared to lean Zucker rats and Sprague-Dawley rats. These findings suggest that dysfunction in the circadian pacemaker previously shown to manifest itself by 43 weeks of age in fatty Zucker rats may already be present at 3 months of age and suggest that altered thermoregulation may play a role in the development of obesity in this animal model of genetic obesity.

Weight reduction increases adipose but decreases cardiac LPL in reduced-obese Zucker rats

1991 ◽  
Vol 261 (2) ◽  
pp. E246-E251 ◽  
Author(s):  
D. H. Bessesen ◽  
A. D. Robertson ◽  
R. H. Eckel
Keyword(s):  
Adipose Tissue ◽  
Cardiac Muscle ◽  
Weight Reduction ◽  
Zucker Rats ◽  
Mrna Levels ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Obese Rats ◽  
Obese Zucker Rats ◽  
Coordinate Changes

Lipoprotein lipase (LPL) activity and mRNA levels were measured in cardiac muscle and adipose tissue from lean, obese, and weight-stable reduced-obese Zucker rats, both fasted and 2 h after feeding. Fasting epididymal fat LPL activity was substantially higher in obese rats relative to lean rats [6.9 vs. 0.2 nmol free fatty acid (FFA).10(6) cells-1.min-1; P = 0.0001], and was higher still in reduced-obese rats (15.7 nmol FFA.10(6) cells-1.min-1; P = 0.002). Adipose tissue LPL increased with feeding in all three groups. In marked contrast, fasting cardiac muscle LPL was lower in obese rats relative to lean (28.8 vs. 38.5 nmol FFA.g-1.min-1; P = 0.0064) and was lower still in reduced-obese rats (14.5 nmol FFA.g-1.min-1; P = 0.0001). LPL mRNA levels increased in adipose tissue along with enzyme activity; however, the magnitude of the changes were relatively small, suggesting that the primary regulatory steps are posttranslational. Weight reduction studies were also carried out in Sprague-Dawley rats with similar results. These studies show that sustained weight reduction results in coordinate changes in tissue-specific LPL, favoring delivery of lipoprotein triglyceride fatty acids to adipose tissue relative to cardiac muscle and the restoration of energy stores.

scholarly journals Milk fermented by Lactobacillus gasseri SBT2055 influences adipocyte size via inhibition of dietary fat absorption in Zucker rats

2008 ◽  
Vol 101 (5) ◽  
pp. 716-724 ◽  
Author(s):  
Essam M. Hamad ◽  
Masao Sato ◽  
Kazunori Uzu ◽  
Takeshi Yoshida ◽  
Seiichiro Higashi ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Dietary Fat ◽  
Zucker Rats ◽  
Fat Absorption ◽  
Adipocyte Size ◽  
Sprague Dawley ◽  
Lactobacillus Gasseri ◽  
Sprague Dawley Rats ◽  
Obese Zucker Rats ◽  
Dietary Fat Absorption

We have demonstrated previously that a diet containing skimmed milk (SM) fermented by Lactobacillus gasseri SBT2055 (LGSP) reduces adipocyte size in Sprague–Dawley rats. Two experiments were conducted to extend these observations in order to elucidate the mechanism involved. In experiment 1, lean and obese Zucker rats were fed a diet containing SM or LGSP for 4 weeks. The LGSP diet, compared with the SM diet, resulted in lowering of the mesenteric adipose tissue weight (23 %; P < 0·05), adipocyte sizes (28 %; P < 0·001) and serum leptin concentration (36 %; P < 0·05) in lean rats. Obese Zucker rats did not display such dietary effects. Only the number of smaller adipocytes was increased (P < 0·05) by the LGSP diet in the subcutaneous adipose tissue of obese rats. The LGSP diet significantly reduced the serum and hepatic cholesterol in rats. In addition, the LGSP diet led to an increased excretion of faecal fatty acids and total neutral faecal sterols in both rat strains. In experiment 2, Sprague–Dawley rats with permanent cannulation of the thoracic duct were fed either the SM or LGSP diets and their lymph was collected. The LGSP diet lowered the maximum transport rate of TAG and phospholipids. These results indicate that fermented milk regulates adipose tissue growth through inhibition at the stage of dietary fat absorption in lean Zucker rats.

scholarly journals Telmisartan prevents the glitazone-induced weight gain without interfering with its insulin-sensitizing properties

2007 ◽  
Vol 293 (1) ◽  
pp. E91-E95 ◽  
Author(s):  
Anne Zanchi ◽  
Abdul G. Dulloo ◽  
Christine Perregaux ◽  
Jean-Pierre Montani ◽  
Michel Burnier
Keyword(s):  
Weight Gain ◽  
Fat Mass ◽  
Zucker Rats ◽  
Peroxisome Proliferator ◽  
Concomitant Treatment ◽  
Sprague Dawley ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ppar Γ ◽  
Sprague Dawley Rats

Glitazones are peroxisome proliferator-activated receptor (PPAR)-γ agonists with powerful insulin-sensitizing properties. They promote the development of metabolically active adipocytes that can lead to a substantial gain in fat mass. Telmisartan is an ANG II type 1 receptor antagonist with partial PPAR-γ agonistic properties. Recently, telmisartan has been reported to prevent weight gain and improve insulin sensitivity in diet-induced obese rodents. The goal of this study was to examine the influence of telmisartan on pioglitazone-induced weight gain and insulin-sensitizing properties in the following two models of insulin resistance: a nongenetic model (high-fat-fed Sprague Dawley rats) and the genetically obese fa/ fa Zucker rat. After a 4-wk treatment, the pioglitazone-induced increase in fat mass was modest in the Sprague Dawley rats and severe in the Zucker rats. In both models, these effects were substantially decreased by concomitant treatment with telmisartan. The effects of telmisartan on body weight and fat mass in the Zucker rats were abolished by pair feeding, suggesting that it is the result of a decrease in food intake. Telmisartan did not interfere with the insulin-sensitizing properties of pioglitazone. This study demonstrates that telmisartan attenuates the glitazone-induced increase in fat mass without interfering with its insulin-sensitizing properties.

scholarly journals Obesity-stimulated aldosterone release is not related to an S1P-dependent mechanism

2017 ◽  
Vol 235 (3) ◽  
pp. 251-265
Author(s):  
Stephan Werth ◽  
Helge Müller-Fielitz ◽  
Walter Raasch
Keyword(s):  
Plasma Aldosterone ◽  
Zucker Rats ◽  
Sprague Dawley ◽  
Aldosterone Secretion ◽  
Sd Rats ◽  
Aldosterone Production ◽  
Sphingosine 1 Phosphate ◽  
H295r Cells ◽  
Obese Zucker Rats

Aldosterone has been identified as an important factor in obesity-associated hypertension. Here, we investigated whether sphingosine-1-phosphate (S1P), which has previously been linked to obesity, increases aldosterone release. S1P-induced aldosterone release was determined in NCI H295R cells in the presence of S1P receptor (S1PR) antagonists. In vivo release of S1P (100–300 µg/kgbw) was investigated in pithed, lean Sprague Dawley (SD) rats, diet-obese spontaneous hypertensive rats (SHRs), as well as in lean or obese Zucker rats. Aldosterone secretion was increased in NCI H295R cells by S1P, the selective S1PR1 agonist SEW2871 and the selective S1PR2 antagonist JTE013. Treatment with the S1PR1 antagonist W146 or fingolimod and the S1PR1/3 antagonist VPbib2319 decreased baseline and/or S1P-stimulated aldosterone release. Compared to saline-treated SD rats, plasma aldosterone increased by ~50 pg/mL after infusing S1P. Baseline levels of S1P and aldosterone were higher in obese than in lean SHRs. Adrenal S1PR expression did not differ between chow- or CD-fed rats that had the highest S1PR1 and lowest S1PR4 levels. S1P induced a short-lasting increase in plasma aldosterone in obese, but not in lean SHRs. However, 2-ANOVA did not demonstrate any difference between lean and obese rats. S1P-induced aldosterone release was also similar between obese and lean Zucker rats. We conclude that S1P is a local regulator of aldosterone production. S1PR1 agonism induces an increase in aldosterone secretion, while stimulating adrenal S1PR2 receptor suppresses aldosterone production. A significant role of S1P in influencing aldosterone secretion in states of obesity seems unlikely.

Uneven blunting of chronotropic baroreflexes in obese Zucker rats

1989 ◽  
Vol 256 (2) ◽  
pp. H417-H421 ◽  
Author(s):  
D. L. Barringer ◽  
R. D. Bunag
Keyword(s):  
Heart Rate ◽  
Female Rats ◽  
Zucker Rats ◽  
Adrenergic Blockade ◽  
Sprague Dawley ◽  
Heart Rates ◽  
Reflex Tachycardia ◽  
Mean Pressure ◽  
Autonomic Blockade ◽  
Obese Zucker Rats

We compared reflex chronotropic responses to intravenously infused drugs in three groups of age-matched normotensive female rats, namely, Sprague-Dawley, lean Zucker, and obese Zucker. Initial mean pressures did not differ between rat groups, but heart rates tended to be lower in obese Zucker rats. Baroreflex impairment was already evident, because heart rate responses to infused phenylephrine (reflex bradycardia) or sodium nitroprusside (reflex tachycardia) were consistently weaker in obese Zucker than in other rats. Regardless of rat grouping, subsequent cholinergic blockade with atropine elevated, whereas beta-adrenergic blockade with propranolol lowered, basal heart rates without affecting mean pressure. Reflex heart rate responses were all appreciably reduced after either type of autonomic blockade, and although the extent of inhibition varied between rat groups, the residual heart rate responses remaining after blockade were nonetheless always smaller in obese than in lean rats. This difference suggests that efferent sympathetic and parasympathetic mechanisms normally responsible for mediating heart rate reflexes were unevenly blunted in obese Zucker rats.

scholarly journals Excessive Weight Gain during Pregnancy Increases Carcinogen-Induced Mammary Tumorigenesis in Sprague-Dawley and Lean and Obese Zucker Rats

2006 ◽  
Vol 136 (4) ◽  
pp. 998-1004 ◽  
Author(s):  
Sonia de Assis ◽  
Mingyue Wang ◽  
Shruti Goel ◽  
Aaron Foxworth ◽  
William Helferich ◽  
...  
Keyword(s):  
Weight Gain ◽  
Mammary Tumorigenesis ◽  
Zucker Rats ◽  
Sprague Dawley ◽  
Excessive Weight Gain ◽  
Excessive Weight ◽  
Obese Zucker Rats ◽  
Weight Gain During Pregnancy
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