Body composition and adiposity in LH-lesioned and pair-fed obese Zucker rats

1982 ◽  
Vol 242 (6) ◽  
pp. E437-E444
Author(s):  
K. M. Milam ◽  
R. E. Keesey ◽  
J. S. Stern
Keyword(s):  
Body Composition ◽  
Body Weight ◽  
Food Restriction ◽  
Cell Number ◽  
Zucker Rats ◽  
Elevated Plasma ◽  
Protein Deposition ◽  
Lean Control ◽  
Obese Rats ◽  
Obese Zucker Rats

It has been reported previously that lateral hypothalamic (LH) lesions alter body composition including reducing adipocyte cellularity in lean and obese Zucker rats. The present experiment was designed to determine whether these alterations in body composition and adipose cell number are secondary to the reduced energy consumption of LH-lesioned rats or to a direct effect of the hypothalamic lesion. Groups of lean and obese Zucker rats, sustaining lesions of the lateral hypothalamus at 10 wk of age, maintained body weight at 72% that of nonlesioned controls until killed at 32 wk. Pair-feeding nonlesioned rats to the intakes of lean and obese LH-lesioned rats produced a reduction in adipocyte number similar to that caused by lesions. However, neither the lean nor obese LH-lesioned rats displayed an increase in cell number when fed a palatable diet that markedly increased carcass lipids. This finding suggests that adipocyte number may be constrained in LH-lesioned rats. These and further observations that 1) lean control rats maintained a higher body weight than the LH-lesioned rats to which they were pair fed and 2) in obese rats, food restriction further reduced protein deposition and elevated plasma insulin relative to comparably fed LH-lesioned obese rats suggest that the LH syndrome is mimicked by simple food restriction.

Effect of swim training on development of obesity in the genetically obese rat

1982 ◽  
Vol 242 (3) ◽  
pp. R204-R211 ◽  
Author(s):  
J. L. Walberg ◽  
P. A. Mole ◽  
J. S. Stern
Keyword(s):  
Body Composition ◽  
Food Restriction ◽  
Plasma Insulin ◽  
Cell Number ◽  
Skeletal Growth ◽  
Zucker Rats ◽  
Fat Cell ◽  
Full Development ◽  
Obese Rats ◽  
Obese Zucker Rats

Seven-week-old female lean and obese Zucker rats were swim trained or kept sedentary for 8 wk. Another group of obese rats was exercised plus food restricted. During exercise training, obese and lean rats ate more but gained less body weight than sedentary controls. Exercise favorably altered body composition, adipose cellularity, and plasma insulin of the obese rat. Exercise plus food restriction more dramatically affected body composition and adipose cellularity but was no more effective in depressing hyperinsulinemia than exercise alone. Following 8 wk of retirement, dorsal fat cell number remained depressed to formerly exercised obese rats whereas adipose cellularity in other depots, body composition, and plasma insulin were similar to control levels. Thus, exercise delayed but did not prevent the full development of obesity in the Zucker rat. Food restriction along with exercise resulted in more permanent effects on adipose cellularity than exercise alone but stunted muscle and skeletal growth.

Scapular brown fat removal enhances development of adiposity in cold-exposed obese Zucker rats

1984 ◽  
Vol 247 (5) ◽  
pp. R918-R926 ◽  
Author(s):  
J. S. Stern ◽  
T. Inokuchi ◽  
T. W. Castonguay ◽  
S. J. Wickler ◽  
B. A. Horwitz
Keyword(s):  
Body Composition ◽  
Weight Gain ◽  
Citrate Synthase ◽  
Body Weight Gain ◽  
Cell Number ◽  
Brown Fat ◽  
Zucker Rats ◽  
Obese Rats ◽  
Fat Removal ◽  
Obese Zucker Rats

To investigate the contribution of brown fat (BAT) to the development of obesity in genetically obese Zucker rats (fa/fa), scapular brown fat (SBAT) was removed from obese and lean 4-wk-old females. Eight weeks after surgery there was no regrowth of SBAT. Lipectomy had no effect on body weight gain, food intake, and body composition when rats were housed at 25 degrees C. Lean rats completely compensated for the lipectomy by increasing BAT mass, protein, cellularity, and activity of citrate synthase (CS) in axillary, perirenal, and thoracic depots. beta-Hydroxyacyl-coenzyme A dehydrogenase (HOAD) activity was increased, but compensation was incomplete. In lipectomized obese rats, only BAT protein and cell number were increased sufficiently for complete compensation. In a second experiment SBAT was removed from obese and lean rats, but rats were housed in the cold (10 degrees C) for 8 wk. In lean rats, although compensation was incomplete, it was sufficient to maintain a weight gain and body composition comparable with sham-operated lean rats. In obese rats, where there was little or no compensation for lipectomy, weight gain and fat deposition were greater than observed in sham-operated obese controls. These data support the hypothesis that reducing the amount of functional BAT contributes to the development of increased adiposity.

scholarly journals Dehydroepiandrosterone Decreases Serum Tumor Necrosis Factor-α and Restores Insulin Sensitivity: Independent Effect from Secondary Weight Reduction in Genetically Obese Zucker Fatty Rats*

Endocrinology ◽  
1998 ◽  
Vol 139 (7) ◽  
pp. 3249-3253 ◽  
Author(s):  
Mari Kimura ◽  
Shun-ichi Tanaka ◽  
Yoshihiko Yamada ◽  
Yoshihiro Kiuchi ◽  
Tadashi Yamakawa ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Insulin Sensitivity ◽  
Tumor Necrosis ◽  
Zucker Rats ◽  
Tnf Α ◽  
Obese Rats ◽  
Obese Zucker Rats ◽  
Dhea Treatment ◽  
Necrosis Factor

Abstract Dehydroepiandrosterone (DHEA) and its sulfate ester are the most abundant circulating adrenal steroids in humans. Administration of DHEA has been reported to have beneficial effects on obesity, hyperlipidemia, diabetes, and atherosclerosis in obese rodents, although its effects on insulin resistance have not been fully elucidated. In this study, the effects of DHEA treatment on insulin sensitivity were investigated in genetically obese Zucker rats, an animal model of insulin resistance, using the euglycemic clamp technique. After 0.4% DHEA was administered for 10 days to female obese Zucker rats aged 16 weeks, body weight and plasma insulin decreased and glucose disposal rate (GDR), which was normally reduced in obese rats, rose significantly compared with age- and sex-matched control obese rats. On the other hand, although the pair-fed obese rats also showed levels of weight reduction similar to those of DHEA-treated rats, the increase in GDR of DHEA-treated rats was significantly greater than in pair-fed rats, suggesting a direct ameliorating effect of DHEA on insulin sensitivity of obese rats. Serum concentration of tumor necrosis factor (TNF)-α, one of cytokines causing insulin resistance, was also reduced significantly in DHEA-treated, but not in pair-fed obese rats. In conclusion, our results suggest that DHEA treatment reduces body weight and serum TNF-α independently, and that both may ameliorate insulin resistance in obese Zucker fatty rats.

Association of fat cell size and paracrine growth factors in development of hyperplastic obesity

1998 ◽  
Vol 275 (6) ◽  
pp. R1898-R1908 ◽  
Author(s):  
Brenda G. Marques ◽  
Dorothy B. Hausman ◽  
Roy J. Martin
Keyword(s):  
Adipose Tissue ◽  
Growth Factors ◽  
Conditioned Medium ◽  
Cellular Proliferation ◽  
Cell Number ◽  
Zucker Rats ◽  
Fat Cell ◽  
Obese Rats ◽  
Paracrine Growth Factors ◽  
Obese Zucker Rats

Inguinal, epididymal, and retroperitoneal adipose tissue from lean and obese Zucker rats, 3–15 wk of age, was used to determine the association among adipocyte size distribution, the presence of paracrine growth factors in adipose tissue, and subsequent changes in adipocyte number. For each specific depot and time point, obese rats had a greater percentage of large adipocytes than did lean rats. A positive correlation ( P < 0.02) was found in obese rats between the percentage of inguinal and epididymal adipocytes in the 140- to 180-μm size range and the ability of conditioned medium prepared from these depots to stimulate cellular proliferation in a bioassay system utilizing preadipocytes from inguinal fat pads of normal rats. Proliferative activity of the conditioned medium from all depots in obese rats was positively correlated ( P < 0.01) to subsequent changes in fat cell number. The data presented here for the inguinal and epididymal depot of obese Zucker rats are consistent with the hypothesis that enlarged adipocytes secrete growth factors that induce preadipocyte proliferation.

scholarly journals Body weight, body composition, and energy metabolism in lean and obese Zucker rats fed soybean oil or butter

2002 ◽  
Vol 75 (1) ◽  
pp. 21-30 ◽  
Author(s):  
Valérie Rolland ◽  
Suzanne Roseau ◽  
Gilles Fromentin ◽  
Stylianos Nicolaidis ◽  
Daniel Tomé ◽  
...  
Keyword(s):  
Body Composition ◽  
Body Weight ◽  
Energy Metabolism ◽  
Soybean Oil ◽  
Zucker Rats ◽  
Obese Zucker Rats

Effect of somatotropin and feed restriction on body composition and adipose metabolism in obese Zucker rats

1995 ◽  
Vol 269 (1) ◽  
pp. E137-E144 ◽  
Author(s):  
M. J. Azain ◽  
D. B. Hausman ◽  
T. R. Kasser ◽  
R. J. Martin
Keyword(s):  
Body Weight ◽  
Body Weight Gain ◽  
Zucker Rats ◽  
Feed Restriction ◽  
Reduced Body ◽  
Obese Zucker Rat ◽  
Obese Rats ◽  
Isolated Adipocytes ◽  
Obese Zucker Rats ◽  
Lean Group

The objective of the present study was to determine whether exogenous somatotropin (STH) administration in conjunction with feed restriction could alter the composition of gain in the obese rat. Five-week-old female lean and obese Zucker rats were assigned to the following treatments for 6 wk: ad libitum fed (AL), restricted (approximately 75% of AL lean), and restricted with STH (2 mg STH/day). Growth rate was decreased in restricted groups and was normalized to that of the AL lean group in restricted rats treated with STH. In lean rats, restriction decreased protein accretion. Restriction plus STH treatment decreased lipid accretion but increased protein accretion and body weight gain compared with the AL lean group. As expected, feed restriction reduced body size in obese rats, but carcass lipid was maintained at 44%, a level similar to that of the AL obese rats. Lipid accretion rate was decreased with restriction in obese rats and was further reduced, to a level similar to that of the lean group, in the obese rats that were restricted and treated with STH. Protein accretion was decreased in the restricted obese group but was normalized in those treated with STH to a level similar to that in the AL lean group. Basal rates of lipolysis in isolated adipocytes were not affected by STH. However, STH treatment normalized the responsiveness of cells from the obese rats to stimulation of lipolysis by isoproterenol. The results demonstrate that a combination of caloric restriction and STH was effective in normalizing body weight and composition of gain in the obese Zucker rat.

Developmental study of adipose cellularity in lateral hypothalamic-lesioned Zucker obese rats

1982 ◽  
Vol 242 (3) ◽  
pp. R311-R317
Author(s):  
K. M. Milam ◽  
R. E. Keesey ◽  
L. H. Storlien ◽  
J. S. Stern
Keyword(s):  
Body Composition ◽  
Zucker Rats ◽  
Specific Response ◽  
Developmental Study ◽  
Adipocyte Size ◽  
Obese Rats ◽  
Electrolytic Lesions ◽  
Obese Zucker Rats ◽  
Percentage Basis ◽  
Absolute Basis

Ten-week-old lean and obese Zucker rats were sham lesioned or received bilateral, electrolytic lesions of the lateral hypothalamus (LH). They were maintained on a wet mash diet until killing at 15 or 32 wk of age; control lean and obese rats were also killed at 6 and 10 wk. Body composition analyses were performed and adipocyte cellularity of epididymal, retroperitoneal, and subcutaneous depots were calculated. Changes in body composition of LH-lesioned rats, though similar in the two genotypes on an absolute basis, differed on a percentage basis due to the extreme adiposity of the obese rats. Retarded development of protein depots in both lesioned lean and obese rats was apparent at 15 but not 32 wk. Relative to genotypic controls, lesioned lean and obese rats had smaller adipose depots by 32 wk due to decreased adipocyte size in lean rats and reduced adipocyte number in the obese. This genotype-specific response was probably due to the chronic hyperplasia of adipocytes unique to the obese rats. This distinctive developmental pattern of the epididymal depot is discussed.

scholarly journals Regulation of the renal thiazide-sensitive Na-Cl cotransporter, blood pressure, and natriuresis in obese Zucker rats treated with rosiglitazone

2005 ◽  
Vol 289 (2) ◽  
pp. F442-F450 ◽  
Author(s):  
Osman Khan ◽  
Shahla Riazi ◽  
Xinqun Hu ◽  
Jian Song ◽  
James B. Wade ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Control Diet ◽  
Zucker Rats ◽  
Receptor Subtype ◽  
Protein Abundance ◽  
Lean Control ◽  
Obese Rats ◽  
Obese Zucker Rats ◽  
Nacl Load

Previously, we showed an increase in protein abundance of the renal thiazide-sensitive Na-Cl cotransporter (NCC) in young, prediabetic, obese Zucker rats relative to lean age mates (Bickel CA, Verbalis JF, Knepper MA, and Ecelbarger CA. Am J Physiol Renal Physiol 281: F639–F648, 2001). To test whether this increase correlated with increased thiazide sensitivity (NCC activity) and blood pressure, and could be modified by insulin-sensitizing agents, we treated lean and obese Zucker rats (9 wk old) with either a control diet or this diet supplemented with 3 mg/kg body wt rosiglitazone (RGZ), a peroxisomal proliferator-activated receptor subtype γ agonist and potent insulin-sensitizing agent, for 12 wk ( n = 9/group). The rise in blood pressure, measured continuously by radiotelemetry, was significantly blunted in the RGZ-treated obese rats. Similarly, blood glucose and urinary albumin were markedly decreased in these rats. RGZ-treated rats whether lean or obese excreted a NaCl load faster but excreted less sodium in response to hydrochlorothiazide, applied as a novel in vivo measure of NCC activity. Obese rats had increased renal protein abundance and urinary excretion of NCC; however, this was not significantly reduced by RGZ (densitometry in cortex homogenate − %lean control): 100 ± 9, 93 ± 4, 124 ± 9, and 141 ± 14 for lean control, lean RGZ, obese control, and obese RGZ, respectively. Subcellular localization, as evaluated by confocal microscopy and immunoblotting following differential centrifugation, of NCC was not different between rat groups. Overall, RGZ reduced blood pressure and thiazide sensitivity; however, the mechanism(s) did not seem to involve a decrease in NCC protein abundance or cellular location. Decreased NCC activity may have contributed to the maintenance of normotension in RGZ-treated obese rats.

Lipoprotein lipase activity and lipolysis after swim training in obese Zucker rats

1983 ◽  
Vol 245 (5) ◽  
pp. R706-R712
Author(s):  
J. L. Walberg ◽  
M. R. Greenwood ◽  
J. S. Stern
Keyword(s):  
Exercise Training ◽  
Lipoprotein Lipase ◽  
Food Restriction ◽  
Plasma Insulin ◽  
Zucker Rats ◽  
Lipoprotein Lipase Activity ◽  
Adipocyte Size ◽  
Metabolic Disturbances ◽  
Obese Rats ◽  
Obese Zucker Rats

Obese and lean Zucker rats, 7 wk old, were swim trained or kept sedentary. Another group of obese rats was food restricted and exercised. Half the rats were killed after training for 8 wk, the remainder were retired and killed after an additional 8 wk. Neither treatment decreased adipocyte size in obese rats. Although basal lipolysis per cell was elevated in obese rats, their adipocytes were insensitive to epinephrine at 15 and 23 wk of age. Exercise training did not affect lipolysis. At all ages, adipose lipoprotein lipase (LPL) capacity was higher in obese relative to lean rats. In obese rats, swim training and exercise plus food restriction increased adipose and gastrocnemius LPL activity and depressed plasma insulin and triglyceride levels. All effects of exercise were transient. Thus, exercise training improved some of the metabolic disturbances in the Zucker obese rat but did not normalize adipocyte size, LPL activity, or lipolysis.

scholarly journals The effect of adrenalectomy on GDP binding to brown-adipose-tissue mitochondria of obese rats

1982 ◽  
Vol 208 (3) ◽  
pp. 819-822 ◽  
Author(s):  
Susan Holt ◽  
David A. York
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Binding Sites ◽  
Zucker Rats ◽  
Lean Control ◽  
Brown Adipose ◽  
Obese Rats ◽  
Number Of Binding Sites ◽  
Obese Zucker Rats

GDP binding to brown-adipose-tissue mitochondria of young obese Zucker rats (fa/fa) was significantly lower than in lean control rats, as a result of a decrease in the number of binding sites. Adrenalectomy of fa/fa rats restored GDP binding to control values. Corticosterone replacement suppressed GDP binding in adrenalectomized obese rats.

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