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

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Dietary Hemp Seeds More Effectively Attenuate Disorders in Genetically Obese Rats than Their Lipid Fraction

Journal of Nutrition ◽

10.1093/jn/nxaa081 ◽

2020 ◽

Vol 150 (6) ◽

pp. 1425-1433 ◽

Cited By ~ 1

Author(s):

Paulina M Opyd ◽

Adam Jurgoński ◽

Bartosz Fotschki ◽

Jerzy Juśkiewicz

Keyword(s):

Lipid Fraction ◽

The Other ◽

Cholesterol Concentration ◽

Liver Cholesterol ◽

Zucker Rats ◽

Standard Diet ◽

Hemp Seed ◽

Hepatic Expression ◽

Obese Rats ◽

Hemp Oil

ABSTRACT Background Hemp seeds are rich in PUFAs and other bioactives that can attenuate the development of obesity-related disorders; however, the extent to which their lipid fraction is responsible for this effect is unknown. Objective We hypothesized that hemp seed or hemp oil supplementation can attenuate genetically determined disorders and that the former are more effective in doing so. Methods Lean and obese male Zucker rats, aged 8 wk, weighing 174 ± 4.2 g and 223 ± 3.8 g, respectively, were allocated to 4 groups. The lean (LC) and obese controls (OC) were fed a standard diet, whereas the other 2 obese groups were fed a modified diet in which hemp oil (4% diet; O + HO) or hemp seeds (12% diet; O + HS) were included. All diets had the same proportions of protein (18%), fat (8%), and fiber (5%) and a similar carbohydrate proportion (∼52%). Diets fed to O + HO and O + HS had similar fatty acid profiles. After 4 wk, markers of gut and liver function, antioxidant status, and lipid metabolism were measured. Results The total SCFA concentration in the cecal digesta was lower in OC (64.8 ± 4.21 µmol/g) compared with LC (78.1 ± 2.83 µmol/g) (P ≤ 0.05), whereas it was greater in O + HS (89 ± 4.41 µmol/g) compared with LC, OC, and O + HO (69.7 ± 2.68 µmol/g) (P ≤ 0.05). Plasma total cholesterol was greater in OC (6.20 ± 0.198 mmol/L) and O + HO (5.60 ± 0.084 mmol/L) compared with LC (2.71 ± 0.094 mmol/L) (P ≤ 0.05); in O + HS, the concentration did not differ from the other groups (5.16 ± 0.278 mmol/L). The liver cholesterol concentration was greater in OC (1.79 ± 0.379 mg/g) compared with the other groups (1.28–1.43 mg/g) (P ≤ 0.05). Hepatic expression of peroxisome proliferator-activated receptor γ was lower in OC (11.9 ± 0.93 units) compared with LC (17.3 ± 1.3 units) (P ≤ 0.05), whereas it was greater in O + HS (19.2 ± 1.04 units) compared with OC and O + HO (14.0 ± 1.33 units) (P ≤ 0.05). Conclusions Dietary hemp seeds more effectively attenuate metabolic disorders in genetically obese rats than the oil extracted from them, which suggests that the lipid fraction is only partly responsible for these effects.

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

British Journal Of Nutrition ◽

10.1079/bjn19880128 ◽

1988 ◽

Vol 60 (3) ◽

pp. 563-569 ◽

Cited By ~ 3

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.

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

AJP Renal Physiology ◽

10.1152/ajprenal.00097.2012 ◽

2012 ◽

Vol 303 (3) ◽

pp. F412-F419 ◽

Cited By ~ 24

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.

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

Acta Endocrinologica ◽

10.1530/eje.1.02046 ◽

2005 ◽

Vol 153 (6) ◽

pp. 963-969 ◽

Cited By ~ 53

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.

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

Biochemical Journal ◽

10.1042/bj2540483 ◽

1988 ◽

Vol 254 (2) ◽

pp. 483-487 ◽

Cited By ~ 21

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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Abstract P184: Co-localization and Natriuretic Interdependence of Angiotensin AT2R and MasR in Obese Rat Kidney

Hypertension ◽

10.1161/hyp.68.suppl_1.p184 ◽

2016 ◽

Vol 68 (suppl_1) ◽

Author(s):

Sanket N Patel ◽

Quaisar Ali ◽

Ulrike Muscha Steckelings ◽

Tahir Hussain

Keyword(s):

Rat Kidney ◽

Sulfhydryl Groups ◽

Zucker Rats ◽

Diabetic Rat ◽

Physical Interaction ◽

Potential Mechanism ◽

Obese Rats ◽

Obese Zucker Rats ◽

Made In

The actions of angiotensin II type 2 receptor (AT 2 R) and receptor mas (MasR) are complex but show similar pro-natriuretic function; particularly AT 2 R expression and natriuretic function are enhanced in obese/diabetic rat kidney. In light of previous reports, we tested hypothesis that AT 2 R and MasR are interdependent to produce natriuresis in obese rats due to potential physical interaction. Infusion of AT 2 R agonist C21 (5 μg/kg/min) in obese Zucker rats (OZR) caused diuresis/natriuresis which were attenuated by simultaneous infusion of the AT 2 R antagonist PD123319 (50 μg/kg/min) or the MasR antagonist A-779 (50 μg/kg/min). Similarly, infusion of MasR agonist Ang-(1-7) (110 fmol/kg/min) in OZR caused diuresis/netriuresis, which were attenuated by simultaneous infusion of A-779 or PD123319. Dual labeling of AT 2 R and MasR in OZR kidney slices revealed four-fold co-localization of AT 2 R and MasR (9.83 vs. 2.50 dual labeled cells/1600 μm 2 ) compared with lean rats in which AT 2 R is not natriuretic. Moreover, the AT 2 R co-immunoprecipitates with MasR in cortical homogenate of OZR. Immunoblotting of AT 2 R and MasR with zero length oxidative (sulfhydryl groups) cross-linker cupric-phenanthroline in OZR cortical homogenate revealed a shift of AT 2 R (~62 kDa) and MasR (~54 kDa) bands upward with overlapping migration for their complexes (~160 kDa and 245 kDa) which were sensitive to the reducing β-mercaptoethanol. Similar observations were made in HK-2 cells, where glucose (25 mM) treatment enhanced the crosslinking. Collectively, the study reveals AT2R and MasR are co-localized and functionally interdependent in producing natriuretic response. Hyperglycemic oxidative stress affecting sulfhydryl groups present a potential mechanism of such physical interaction between these receptors. (Support: R01DK061578)

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Effect of hypophysectomy on energy balance and brown fat activity in obese Zucker rats

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1988.254.2.e162 ◽

1988 ◽

Vol 254 (2) ◽

pp. E162-E166

Author(s):

S. Holt ◽

N. J. Rothwell ◽

M. J. Stock ◽

D. A. York

Keyword(s):

Energy Balance ◽

Binding Capacity ◽

Zucker Rats ◽

Bat Activity ◽

Reduced Body ◽

Brown Adipose ◽

Obese Rats ◽

Obese Zucker Rats ◽

Energy Gains ◽

Pituitary Adrenal Axis

Hypophysectomy (HYPX) in genetically obese (fa/fa) Zucker rats significantly reduced body weight and energy gains and stimulated energy expenditure (by 34%), the thermic response to food (by 144%), and brown adipose tissue (BAT) mitochondrial GDP-binding capacity (by 190%) compared with pair-fed, sham-operated obese rats. These changes in energy balance in obese HYPX rats were reversed by corticosterone replacement (1 mg/day), but the increased BAT activity was only partly restored to normal. HYPX had only small effects on energy balance in lean Zucker rats compared with pair-fed, sham-operated lean controls but increased the acute thermic response to food and BAT mitochondrial GDP-binding capacity; these effects were inhibited by replacement of HYPX rats with corticosterone. The results suggest that alterations in the hypothalamic-pituitary-adrenal axis play a fundamental role in the development and maintenance of genetic obesity.

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Relationship of adipocyte size to hyperphagia in developing male obese Zucker rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1992.262.1.r33 ◽

1992 ◽

Vol 262 (1) ◽

pp. R33-R38 ◽

Cited By ~ 1

Author(s):

J. R. Vasselli ◽

J. A. Fiene ◽

C. A. Maggio

Keyword(s):

Adipose Tissue ◽

Body Weight Gain ◽

Zucker Rats ◽

Lipoprotein Lipase Activity ◽

Adipocyte Size ◽

High Fat ◽

Obese Rats ◽

Obese Zucker Rats ◽

Relationship Of ◽

Cumulative Intake

In growing male obese Zucker rats, hyperphagia reaches a maximum or “breakpoint” and declines at an earlier age with high fat than with chow-type diets. A serial adipose tissue biopsy technique was used to correlate changes of retroperitoneal adipocyte size and feeding behavior in 5- to 7-wk-old male lean and obese rats fed laboratory chow or a 35% fat diet until 30 wk of age. Although chow-fed groups had significantly greater cumulative intake, fat-fed groups had significantly greater body weight gain, retroperitoneal depot weight, and adipocyte number. Mean adipocyte size increased continuously in chow-fed groups but decreased over weeks 20-30 in fat-fed groups, reflecting increased adipocyte number. In fat-fed obese rats, hyperphagia reached a breakpoint at 11 wk and disappeared by 13 wk. In chow-fed obese rats, hyperphagia reached a breakpoint at 15-16 wk and disappeared by 19 wk. Biopsy samples revealed that adipocyte size of fat-fed obese rats was already close to maximal at 10 wk (1.12 micrograms lipid), while that of chow-fed obese rats only approached maximal at 20 wk (0.81 microgram lipid). At these time points, lipoprotein lipase activity paralleled adipocyte size. These data indicate that the duration of the growing obese rat's hyperphagia coincides with adipocyte filling and suggest the existence of feeding stimulatory and inhibitory signals from adipose tissue.

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Mechanism controlling sleep organization of the obese Zucker rats

Journal of Applied Physiology ◽

10.1152/jappl.1998.84.1.253 ◽

1998 ◽

Vol 84 (1) ◽

pp. 253-256 ◽

Cited By ~ 29

Author(s):

David Megirian ◽

Jacek Dmochowski ◽

Gaspar A. Farkas

Keyword(s):

Eye Movement ◽

Rem Sleep ◽

Nrem Sleep ◽

Zucker Rats ◽

Rapid Eye Movement ◽

Zucker Rat ◽

Obese Zucker Rat ◽

Obese Rats ◽

Obese Zucker Rats ◽

The Mean

Megirian, David, Jacek Dmochowski, and Gaspar A. Farkas. Mechanism controlling sleep organization of the obese Zucker rat. J. Appl. Physiol. 84(1): 253–256, 1998.—We tested the hypothesis that the obese ( fa/fa) Zucker rat has a sleep organization that differs from that of lean Zucker rats. We used the polygraphic technique to identify and to quantify the distribution of the three main states of the rat: wakefulness (W), non-rapid-eye-movement (NREM), and rapid-eye-movement (REM) sleep states. Assessment of states was made with light present (1000–1600), at the rats thermoneutral temperature of 29°C. Obese rats, compared with lean ones, did not show significant differences in the total time spent in the three main states. Whereas the mean durations of W and REM states did not differ statistically, that of NREM did ( P = 0.046). However, in the obese rats, the frequencies of switching from NREM sleep to W, which increased, and from NREM to REM sleep, which decreased, were statistically significantly different ( P = 0.019). Frequency of switching from either REM or W state was not significantly different. We conclude that sleep organization differs between lean and obese Zucker rats and that it is due to a disparity in switching from NREM sleep to either W or REM sleep and the mean duration of NREM sleep.

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