scholarly journals The effects of dietary fat content on the growth and body composition of lean and genetically obese Zucker rats adrenalectomized before weaning

1988 ◽  
Vol 60 (3) ◽  
pp. 563-569 ◽  
Author(s):  
J. M. Fletcher ◽  
N. McKenzie
Keyword(s):  
Body Composition ◽  
Dietary Fat ◽  
The Body ◽  
Zucker Rats ◽  
Stock Diet ◽  
Phenotypic Difference ◽  
Body Lipid ◽  
Body Protein ◽  
Obese Rats ◽  
Obese Zucker Rats

1. Lean (Fa/–) and obese (fa/fa) Zucker rats were adrenalectomized or sham-operated at 18 d of age (3 d before weaning). After weaning the rats were fed ad lib. on semi-synthetic diets containing either a low (8 g/kg) or a high (178 g/kg) proportion of fat. Other groups of sham-operated rats were given the same amount eaten by adrenalectomized animals (restricted intake). Rats were killed at 40 d of age.2. Adrenalectomy reduced the body lipid content of lean and obese rats compared with intact animals fed ad lib. or given a restricted intake. Adrenalectomized obese rats contained more body lipid than intact or adrenalectomized lean rats.3. Sham-operated obese rats given a restricted intake had less body protein than similarly treated lean animals and this phenotypic difference was abolished by adrenalectomy.4. There were no effects of diet on growth or body composition of intact or adrenalectomized rats.5. It is concluded that preweaning adrenalectomy prevented development of the obese phenotype when rats were fed on either diet. Comparison of these results with a previous study, in which adrenalectomized Zucker rats were fed on a stock diet (Fletcher, 1986b), showed, however, that feeding either of the semi-synthetic diets caused greater deposition of body lipid in obese rats.

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.

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.

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 The fate of 14C derived from radioactively labelled dietary precursors in young rats of the Zucker strain (Fa/- and fa/fa)

1986 ◽  
Vol 235 (2) ◽  
pp. 323-327 ◽  
Author(s):  
P Haggarty ◽  
P J Reeds ◽  
J M Fletcher ◽  
K W J Wahle
Keyword(s):  
Tricarboxylic Acid Cycle ◽  
Essential Amino Acids ◽  
Tricarboxylic Acid ◽  
High Rate ◽  
Zucker Rats ◽  
Metabolic Fate ◽  
Phenotypic Difference ◽  
Body Lipid ◽  
Protein Deposition ◽  
Obese Zucker Rats

The metabolic fate of 14C derived from radioactively labelled dietary precursors was determined in immature (18- and 25-day-old) lean and obese Zucker rats. This included measurement of 14C incorporated into body lipid, non-essential amino acids and expired CO2. Before weaning (18 days) there was no phenotypic difference between the fates of [14C]palmitate and [14C]-glucose. However, after weaning (25 days) all the precursors studied exhibited an increase in the fraction incorporated into lipid in the obese rat as compared with the lean animal. This was reflected in the fate of acetyl-CoA in the tricarboxylic acid cycle. There was little phenotypic difference in the fraction of leucine or valine catabolized. The results presented here suggest that the high rate of lipogenesis found in the obese rat is supported by carbon from all the dietary precursors studied. It is also argued that the decreased protein deposition found in the obese rat is not caused by the high rate of lipogenesis removing precursors for protein synthesis, as has been suggested elsewhere [Cleary, Vasselli & Greenwood (1980) Am. J. Physiol. 238, E284-E292].

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 Comparative Effects of Dietary Hemp and Poppy Seed Oil on Lipid Metabolism and the Antioxidant Status in Lean and Obese Zucker Rats

Molecules ◽  
2020 ◽  
Vol 25 (12) ◽  
pp. 2921
Author(s):  
Bartosz Fotschki ◽  
Paulina Opyd ◽  
Jerzy Juśkiewicz ◽  
Wiesław Wiczkowski ◽  
Adam Jurgoński
Keyword(s):  
Lipid Metabolism ◽  
Antioxidant Status ◽  
Seed Oil ◽  
The Body ◽  
Liver Cholesterol ◽  
Zucker Rats ◽  
Poppy Seed ◽  
Hemp Seed ◽  
Obese Rats ◽  
Obese Zucker Rats

The objective of this study was to compare the effects of the dietary inclusion of hemp seed oil (HO) and poppy seed oil (PO) on the lipid metabolism and antioxidant status of lean and genetically obese Zucker rats. The rats were fed a control diet for laboratory rodents or a modification with HO or PO. Both oils reduced body and epididymal fat and liver cholesterol levels and promoted oxidative stress in the liver of obese rats. The HO reduced plasma triglycerides and had a stronger liver cholesterol-lowering effect in obese rats than PO. In the lean rats, HO and PO had no effects on the body fat content, plasma lipid profile, or lipid metabolism in the liver. HO considerably elevated the content of α-linolenic acid in the liver and increased the liver ratio of reduced glutathione (GSH)/oxidized glutathione (GSSG) in the lean rats. In conclusion, the regular consumption of both oils increases the accumulation of essential fatty acids in the liver of healthy animals, whilst not having any adverse effects on the body, whereas in genetically obese rats, the effects of both dietary oils on the lipid metabolism and antioxidant status are unequivocal and only partially beneficial.

scholarly journals Tissue and whole-body protein synthesis in immature Zucker rats and their relationship to protein deposition

1982 ◽  
Vol 204 (2) ◽  
pp. 393-398 ◽  
Author(s):  
P J Reeds ◽  
P Haggarty ◽  
K W J Wahle ◽  
J M Fletcher
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Post Partum ◽  
The Body ◽  
Whole Body ◽  
Zucker Rats ◽  
Body Protein ◽  
Protein Deposition ◽  
Fractional Rate ◽  
Obese Rats

The rates of protein synthesis in skeletal muscle, intestine, liver and in the whole body of immature (18 and 25 days old) lean and obese male Zucker rats were measured. In addition, the rate of deposition of whole-body and skeletal-muscle protein over the period 16-27 days post partum was measured by comparative slaughter and analysis of the composition of the body. At 16 days post partum, lean and obese rats had similar body protein contents, but thereafter the rate of protein deposition in the body and skeletal-muscle mass was decreased in the obese rats. The decrease was particularly marked before 21 days of age, and between 23 and 27 days post partum the fractional rate of protein deposition was the same in lean and obese rats. Of the tissues that were studied, only skeletal muscle had a lower fractional rate of protein synthesis in the obese rats. At 18 days post partum, the decrease in the absolute rate of protein synthesis in skeletal muscle accounted for at least 80% of the decline in protein synthesis in the whole body. After weaning, phenotypic differences in protein synthesis was less marked than at 18 days of age, and skeletal muscle accounted for only 50% of the difference in body protein synthesis between phenotypes. The possibility that a change in the function of the adrenal cortex contributes to differences in protein metabolism between lean and obese Zucker rats is discussed.

scholarly journals High Na intake increases renal angiotensin II levels and reduces expression of the ACE2-AT2R-MasR axis in obese Zucker rats

2012 ◽  
Vol 303 (3) ◽  
pp. F412-F419 ◽  
Author(s):  
Preethi Samuel ◽  
Quaisar Ali ◽  
Rifat Sabuhi ◽  
Yonnie Wu ◽  
Tahir Hussain
Keyword(s):  
Sodium Intake ◽  
Zucker Rats ◽  
Kidney Cortex ◽  
Complex Nature ◽  
Ang Ii ◽  
Pronounced Increase ◽  
High Sodium ◽  
High Sodium Intake ◽  
Obese Rats ◽  
Obese Zucker Rats

High sodium intake is known to regulate the renal renin-angiotensin system (RAS) and is a risk factor for the pathogenesis of obesity-related hypertension. The complex nature of the RAS reveals that its various components may have opposing effects on natriuresis and blood pressure regulation. We hypothesized that high sodium intake differentially regulates and shifts a balance between opposing components of the renal RAS, namely, angiotensin-converting enzyme (ACE)-ANG II-type 1 ANG II receptor (AT1R) vs. AT2-ACE2-angiotensinogen (Ang) (1–7)-Mas receptor (MasR), in obesity. In the present study, we evaluated protein and/or mRNA expression of angiotensinogen, renin, AT1A/BR, ACE, AT2R, ACE2, and MasR in the kidney cortex following 2 wk of a 8% high-sodium (HS) diet in lean and obese Zucker rats. The expression data showed that the relative expression pattern of ACE and AT1BR increased, renin decreased, and ACE2, AT2R, and MasR remained unaltered in HS-fed lean rats. On the other hand, HS intake in obese rats caused an increase in the cortical expression of ACE, a decrease in ACE2, AT2R, and MasR, and no changes in renin and AT1R. The cortical levels of ANG II increased by threefold in obese rats on HS compared with obese rats on normal salt (NS), which was not different than in lean rats. The HS intake elevated mean arterial pressure in obese rats (27 mmHg) more than in lean rats (16 mmHg). This study suggests that HS intake causes a pronounced increase in ANG II levels and a reduction in the expression of the ACE2-AT2R-MasR axis in the kidney cortex of obese rats. We conclude that such changes may lead to the potentially unopposed function of AT1R, with its various cellular and physiological roles, including the contribution to the pathogenesis of obesity-related hypertension.

scholarly journals Plasma calcitonin gene-related peptide is increased prior to obesity, and sensory nerve desensitization by capsaicin improves oral glucose tolerance in obese Zucker rats

2005 ◽  
Vol 153 (6) ◽  
pp. 963-969 ◽  
Author(s):  
Dorte X Gram ◽  
Anker J Hansen ◽  
Michael Wilken ◽  
Torben Elm ◽  
Ove Svendsen ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Tolerance ◽  
Sensory Nerve ◽  
Zucker Rats ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
Nerve Activity ◽  
Calcitonin Gene ◽  
Obese Rats ◽  
Obese Zucker Rats

Objective: It has earlier been demonstrated that capsaicin-induced desensitization improves insulin sensitivity in normal rats. However, whether increased capsaicin-sensitive nerve activity precedes the onset of insulin resistance in diet-induced obesity – and therefore might be involved in the pathophysiology – is not known. Further, it is of relevance to investigate whether capsaicin desensitization improves glycaemic control even in obese individuals and we therefore chose the obese Zucker rats to test this. Design and methods: Plasma levels of calcitonin gene-related peptide (CGRP; a marker of sensory nerve activity) was assessed in 8-week-old Zucker rats. To investigate whether capsaicin desensitization (100 mg/kg at 9 weeks of age) would also ameliorate glycaemia in this non-diabetic model, we assessed oral glucose tolerance at 7 weeks after capsaicin. Results: It was found that plasma CGRP levels were elevated in obese Zucker rats prior to the onset of obesity (16.1±3.4 pmol/l in pre-obese Zucker rats vs 6.9±1.1 pmol/l in lean littermates; P = 0.015) despite similar body weights. Furthermore, capsaicin desensitization reduced both fasting blood glucose (4.3±0.2 mmol/l vs 5.1±0.2 mmol/l in controls; P = 0.050) as well as the mean blood glucose level during an oral glucose tolerance test (OGTT) (6.8±0.3 mmol/l vs 8.6±0.5 mmol/l in control obese rats; P = 0.024) whereas the plasma insulin levels during the OGTT were unchanged. However this did not lead to an improvement in insulin resistance or to a reduction of tissue triglyceride accumulation in muscle or liver. Conclusion: We concluded that capsaicin-induced sensory nerve desensitization improves glucose tolerance in Zucker rats. Since, in this study, plasma CGRP levels, a marker of sensory nerve activity, were increased in the pre-obese rats, our data support the hypothesis that increased activity of sensory nerves precedes the development of obesity and insulin resistance in Zucker rats.

scholarly journals Adipose-tissue-specific increase in glyceraldehyde-3-phosphate dehydrogenase activity and mRNA amounts in suckling pre-obese Zucker rats. Effect of weaning

1988 ◽  
Vol 254 (2) ◽  
pp. 483-487 ◽  
Author(s):  
I Dugail ◽  
A Quignard-Boulange ◽  
R Bazin ◽  
X Le Liepvre ◽  
M Lavau
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Zucker Rats ◽  
Tissue Specific ◽  
Gapdh Gene ◽  
Gapdh Activity ◽  
Weanling Rats ◽  
Obese Rats ◽  
Specific Increase ◽  
Obese Zucker Rats

The regulation of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) gene expression was studied during the onset of obesity in the genetically obese (fa/fa) rat by determination of GAPDH activity and hybridizable mRNA amounts in adipose tissue and liver from suckling and weanling rats. GADPH activity remained low throughout the suckling period, and a burst of activity occurred after weaning in both lean and obese pups. As early as 7 days of age, adipose tissue from pre-obese rats displayed a significant increase in enzyme activity, whereas no difference could be detected in the liver. In both suckling (16 days of age) and weanling (30 days of age) obese rats a proportionate increase in GAPDH activity and mRNA amounts was observed in adipose tissue, but not in liver. It is concluded that the obese genotype influences GAPDH gene expression at a pretranslational level and in a tissue-specific manner. This phenomenon could partly contribute to the hyperactive fat accretion in the obese rat, since glycolysis is the major metabolic pathway for lipogenic substrates in adipose tissue.

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