Docosahexaenoic Acid at 0.4% of Dietary Weight Enhances Lean Mass in Young Female Sprague-Dawley Rats

2019 ◽  
Vol 149 (3) ◽  
pp. 479-487 ◽  
Author(s):  
Zahra Farahnak ◽  
Julia Lévy-Ndejuru ◽  
Paula Lavery ◽  
Hope A Weiler

ABSTRACT Background Docosahexaenoic acid (DHA; 22:6n–3) is an n–3 (ω-3) fatty acid known for beneficial effects on body composition. Objective The objective of the study was to test the dose response of lean and fat mass to DHA in healthy growing female rats. Methods Female Sprague-Dawley rats (7 wk at baseline; n = 12/diet) were randomly assigned to receive a control (AIN-93M; 60 g soybean oil/kg diet) or experimental diet for 10 wk. Experimental diets contained 0.1%, 0.4%, 0.8%, or 1.2% DHA (wt:wt of total diet). Imaging for whole-body and abdominal composition was conducted using dual-energy X-ray absorptiometry and microcomputed tomography, respectively, at weeks 0, 5, and 10. Fatty acid profiles of several tissues were analyzed using gas chromatography. Serum leptin, C-reactive protein, and plasma insulin-like growth factor I concentrations were measured at each time point using immunoassays. Data were tested using Pearson's correlations and mixed-model ANOVA. Results No differences were observed in weight at baseline or food intake throughout the study. Overall, a 6% increase (P < 0.05) in whole-body and abdominal lean mass was observed in the 0.4%-DHA diet group compared with the control diet group. Moreover, the abdominal visceral fat mass was 31.4% lower in rats in the 0.4%-DHA than in the 1.2%-DHA diet group (P < 0.001). Rats in the 1.2%-DHA diet group showed greater percent differences in whole-body (32.5% and 40.6% higher) and in abdominal (33.9% and 49.4% higher) fat mass relative to the 0.1%- and 0.4%-DHA diet groups, respectively (P < 0.01). Accordingly, serum leptin concentration was lower in the 0.1%-DHA (38.2%) and 0.4%-DHA (43.8%) diet groups (P < 0.01) than in the 1.2%-DHA diet group and positively related to whole-body fat mass (r = 0.91, P < 0.0001). Conclusion Dietary DHA at 0.4% of dietary weight effectively enhances lean mass and proportionally reduces fat mass in growing female rats.

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Md Mustahsan Billah ◽  
Saroj Khatiwada ◽  
Virginie Lecomte ◽  
Margaret Morris ◽  
Chris Maloney

Abstract Objectives Emerging evidence suggests that paternal obesity plays a significant role on offspring health. Our previous work in rodents showed that high fat diet (HFD) induced paternal obesity reduced offspring glucose tolerance. It has also been reported that paternal obesity can initiate metabolic disturbance in subsequent generations. Therefore, we designed a novel micronutrient supplement to ameliorate the transgenerational effects of paternal obesity. Methods Founder (F0) male Sprague Dawley rats (3 weeks, 12 per group) were weaned on control (CD) or HFD or diets containing micronutrient supplement (CS; HS), after which they were mated with CD fed females at 19 weeks of age. Twelve F1 offspring from each litter across the four diet groups were weaned on day 21 onto CD, generating four F1 groups. After 14 weeks on CD, they were mated with CD fed females. Male F2 siblings were fed CD or HFD from day 21. After 6 weeks on diet, they underwent EchoMRI (See attached study design). Results HFD increased adiposity (CD: 12.3%, HFD: 18.6%) in F0 which was normalized by supplementation (HS: 11.7%). Though no paternal effect on adiposity was found in F1 males across the four groups, supplementing F0 had significant impact on F2 body composition (fat mass, fat and lean percentage) without influencing body weight and lean mass after 6 weeks on diet. In F2, post weaning HFD significantly increased fat mass in rats from CD and HFD fed founders (CH vs CC P = 0.0001; HH vs HC P = 0.009) but this effect was significantly reduced by F0 supplementation irrespective of F0 diets (CSH vs CH P = 0.017; and HSH vs HH P = 0.04) [3-way ANOVA][See attached table]. Moreover, lean percentage was decreased by post weaning HFD in rats from both non-supplemented F0 diet groups but interestingly this effect was significantly reduced only in rats sired by supplemented CD fed F0 (CSH > CH; P = 0.04). Conclusions Supplementing CD fed grandfathers ameliorated the deleterious effect of HFD, decreasing fat deposition and increasing lean percentage whereas supplementing HFD fed F0 reduced only fat deposition without affecting lean mass of male grand offspring. Therefore, our designed supplement could eventually reduce the transgenerational effect of paternal obesity. Funding Sources Supported by Australian NHMRC grant to MJM and CAM; MMB is supported by Scientia PhD Scholarship, UNSW. Supporting Tables, Images and/or Graphs


1997 ◽  
Vol 16 (2) ◽  
pp. 89-100 ◽  
Author(s):  
W. Sontag ◽  
R. Wirth ◽  
A. Luz ◽  
E. Schäffer ◽  
V. Volf

Female Sprague-Dawley rats, 10-12-week old and weigh ing about 240 g, were injected intravenously with 237Np nitrate. In the toxicological study 77 rats served as controls and 28 rats per group received single doses of 5.2 and 26 kBq, respectively, per kg body weight. In addition, 12 rats of each injection level, sacrificed at defined points in time, were used for dosimetric studies. During the whole life-span the body weight and 237Np whole body-content of each animal were recorded. After death a detailed pathological examination was made of each animal in the cronical study. One day after injection 48% of the injected activity was in the skeleton, 9.3% in the liver, 3% in the kidneys and 4.4% in the rest of the organs. Whereas in all organs the activity decreased very fast, the half-life in the skeleton was about 1400 days. The bodyweights were comparable in the three groups, but the life span decreased from 800 days (control group) to 644 days after injection (26 kBq kg -1 body weight group). The main lesions in the female rats were mammary tumors (73%) and pituitary gland tumors (52%). With increasing activity the incidence of pituary gland tumors decreased and that of osteosarco mas increased from 1.3% (control group) to 32% (26 kBq kg-1 body weight group), whereas the remaining lesions showed no influence on the activity.


2009 ◽  
Vol 106 (4) ◽  
pp. 1100-1111 ◽  
Author(s):  
A. Guadalupe-Grau ◽  
J. Perez-Gomez ◽  
H. Olmedillas ◽  
J. Chavarren ◽  
C. Dorado ◽  
...  

Leptin and osteocalcin play a role in the regulation of the fat-bone axis and may be altered by exercise. To determine whether osteocalcin reduces fat mass in humans fed ad libitum and if there is a sex dimorphism in the serum osteocalcin and leptin responses to strength training, we studied 43 male (age 23.9 2.4 yr, mean ± SD) and 23 female physical education students (age 23.2 ± 2.7 yr). Subjects were randomly assigned to two groups: training (TG) and control (CG). TG followed a strength combined with plyometric jumps training program during 9 wk, whereas the CG did not train. Physical fitness, body composition (dual-energy X-ray absorptiometry), and serum concentrations of hormones were determined pre- and posttraining. In the whole group of subjects (pretraining), the serum concentration of osteocalcin was positively correlated ( r = 0.29–0.42, P < 0.05) with whole body and regional bone mineral content, lean mass, dynamic strength, and serum-free testosterone concentration ( r = 0.32). However, osteocalcin was negatively correlated with leptin concentration ( r = −0.37), fat mass ( r = −0.31), and the percent body fat ( r = −0.44). Both sexes experienced similar relative improvements in performance, lean mass (+4–5%), and whole body (+0.78%) and lumbar spine bone mineral content (+1.2–2%) with training. Serum osteocalcin concentration was increased after training by 45 and 27% in men and women, respectively ( P < 0.05). Fat mass was not altered by training. Vastus lateralis type II MHC composition at the start of the training program predicted 25% of the osteocalcin increase after training. Serum leptin concentration was reduced with training in women. In summary, while the relative effects of strength training plus plyometric jumps in performance, muscle hypertrophy, and osteogenesis are similar in men and women, serum leptin concentration is reduced only in women. The osteocalcin response to strength training is, in part, modulated by the muscle phenotype (MHC isoform composition). Despite the increase in osteocalcin, fat mass was not reduced.


2015 ◽  
Vol 5 (4) ◽  
pp. 127-136
Author(s):  
Ali S. H. Alchalabi ◽  
Erkihun Aklilu ◽  
Abd Rahman Aziz ◽  
F. Malek ◽  
S. H. Ronald ◽  
...  

  In the current study, the effect of 1800 MHz radiofrequency radiation exposure on female rats’ fertility was investigated. The study was conducted on the nine groups of female Sprague-Dawley rats (20 rats/group) with a control group and exposure groups which exposed to EMF 1hr/day and 2hr/day for 15, 30 and 60 days respectively. Animals were whole-body exposed using a GSM-like radiofrequency generator at SAR level 0.048 W/Kg. After the last exposure, rats were divided into two subgroups for fertility evaluation, ovari-an follicle count, and oxidative stress assessment. Prolonged cohabitation day until delivery in exposure groups animals compared to control was ob-served. Moreover, a significant decrease in the number of pups per delivery was observed. Ovarian follicle count showed a dramatic decrease in exposure groups throughout the experiment except the number of atretic follicles was significantly increased compared to control groups. FSH level was signifi-cantly reduced within exposure groups. LH level remained constant except in 2hr. /day group for 60 days. Melatonin levels were significantly lower in ex-posure groups. Glutathione peroxidase activity was reduced in most exposure groups. Malondialdehyde levels were raised significantly in most expo-sure groups compared to the control. Our findings conclude that exposure to electromagnetic field's cause female reproductive activity impairment.


2011 ◽  
Vol 300 (5) ◽  
pp. H1781-H1787 ◽  
Author(s):  
Sachin S. Kandlikar ◽  
Gregory D. Fink

Excess sympathetic nervous system activity (SNA) is linked to human essential and experimental hypertension. To test whether sympathetic activation is associated with a model of deoxycorticosterone acetate (DOCA)-salt hypertension featuring two kidneys and a moderate elevation of blood pressure, we measured whole body norepinephrine (NE) spillover as an index of global SNA. Studies were conducted in chronically catheterized male Sprague-Dawley rats drinking water containing 1% NaCl and 0.2% KCl. After a 7-day surgical recovery and a 3-day control period, a DOCA pellet (50 mg/kg) was implanted subcutaneously in one group of rats (DOCA), while the other group underwent sham implantation (Sham). NE spillover was measured on control day 2 and days 7 and 14 after DOCA administration or sham implantation. During the control period, mean arterial pressure (MAP) was similar in Sham and DOCA rats. MAP was significantly increased in the DOCA group compared with the Sham group after DOCA administration ( day 14: Sham = 109 ± 5.3, DOCA = 128 ± 3.6 mmHg). However, plasma NE concentration, clearance, and spillover were not different in the two groups at any time. To determine whether selective sympathetic activation to the kidneys contributes to hypertension development, additional studies were performed in renal denervated (RDX) and sham-denervated (Sham-DX) rats. MAP, measured by radiotelemetry, was similar in both groups during the control and DOCA treatment periods. In conclusion, global SNA is not increased during the development of mild DOCA-salt hypertension, and fully intact renal nerves are not essential for hypertension development in this model.


2002 ◽  
Vol 282 (3) ◽  
pp. E593-E600 ◽  
Author(s):  
Gregory R. Steinberg ◽  
Arend Bonen ◽  
David J. Dyck

Leptin acutely increases fatty acid (FA) oxidation and triacylglycerol (TG) hydrolysis and decreases TG esterification in oxidative rodent muscle. However, the effects of chronic leptin administration on FA metabolism in skeletal muscle have not been examined. We hypothesized that chronic leptin treatment would enhance TG hydrolysis as well as the capacity to oxidize FA in soleus (SOL) muscle. Female Sprague-Dawley rats were infused for 2 wk with leptin (LEPT; 0.5 mg · kg−1 · day−1) by use of subcutaneously implanted miniosmotic pumps. Control (AD-S) and pair-fed (PF-S) animals received saline-filled implants. Subsequently, FA metabolism was monitored for 45 min in isolated, resting, and contracting (20 tetani/min) SOL muscles by means of pulse-chase procedures. Food intake (−33 ± 2%, P < 0.01) and body mass (−12.5 ± 4%, P = 0.01) were reduced in both LEPT and PF-S animals. Leptin levels were elevated (+418 ± 7%, P < 0.001) in treated animals but reduced in PF-S animals (−73 ± 8%, P< 0.05) relative to controls. At rest, TG hydrolysis was increased in leptin-treated rats (1.8 ± 2.2, AD-S vs. 23.5 ± 8.1 nmol/g wet wt, LEPT; P < 0.001). In contracting SOL muscles, TG hydrolysis (1.5 ± 0.6, AD-S vs. 3.6 ± 1.0 μmol/g wet wt, LEPT; P = 0.02) and palmitate oxidation (18.3 ± 6.7, AD-S vs. 45.7 ± 9.9 nmol/g wet wt, LEPT; P < 0.05) were both significantly increased by leptin treatment. Chronic leptin treatment had no effect on TG esterification either at rest or during contraction. Markers of overall (citrate synthase) and FA (hydroxyacyl-CoA dehydrogenase) oxidative capacity were unchanged with leptin treatment. Protein expression of hormone-sensitive lipase (HSL) was also unaltered following leptin treatment. Thus leptin-induced increases in lipolysis are likely due to HSL activation (i.e., phosphorylation). Increased FA oxidation secondary to chronic leptin treatment is not due to an enhanced oxidative capacity and may be a result of enhanced flux into the mitochondrion (i.e., carnitine palmitoyltransferase I regulation) or electron transport uncoupling (i.e., uncoupling protein-3 expression).


2001 ◽  
Vol 91 (4) ◽  
pp. 1828-1835 ◽  
Author(s):  
Nicole Stupka ◽  
Peter M. Tiidus

The effects of estrogen and ovariectomy on indexes of muscle damage after 2 h of complete hindlimb ischemia and 2 h of reperfusion were investigated in female Sprague-Dawley rats. The rats were assigned to one of three experimental groups: ovariectomized with a 17β-estradiol pellet implant (OE), ovariectomized with a placebo pellet implant (OP), or control with intact ovaries (R). It was hypothesized that following ischemia-reperfusion (I/R), muscle damage indexes [serum creatine kinase (CK) activity, calpain-like activity, inflammatory cell infiltration, and markers of lipid peroxidation (thiobarbituric-reactive substances)] would be lower in the OE and R rats compared with the OP rats due to the protective effects of estrogen. Serum CK activity following I/R was greater ( P < 0.01) in the R rats vs. OP rats and similar in the OP and OE rats. Calpain-like activity was greatest in the R rats ( P < 0.01) and similar in the OP and OE rats. Neutrophil infiltration was assessed using the myeloperoxidase (MPO) assay and immunohistochemical staining for CD43-positive (CD43+) cells. MPO activity was lower ( P < 0.05) in the OE rats compared with any other group and similar in the OP and R rats. The number of CD43+ cells was greater ( P < 0.01) in the OP rats compared with the OE and R rats and similar in the OE and R rats. The OE rats had lower ( P < 0.05) thiobarbituric-reactive substance content following I/R compared with the R and OP rats. Indexes of muscle damage were consistently attenuated in the OE rats but not in the R rats. A 10-fold difference in serum estrogen content may mediate this. Surprisingly, serum CK activity and muscle calpain-like activity were lower ( P< 0.05) in the OP rats compared with the R rats. Increases in serum insulin-like growth factor-1 content ( P < 0.05) due to ovariectomy were hypothesized to account for this finding. Thus both ovariectomy and estrogen supplementation have differential effects on indexes of I/R muscle damage.


2009 ◽  
Vol 87 (6) ◽  
pp. 460-470 ◽  
Author(s):  
Claude Lajoie ◽  
Viviane El-Helou ◽  
Cindy Proulx ◽  
Robert Clément ◽  
Hugues Gosselin ◽  
...  

Rapamycin represents a recognized drug-based therapeutic approach to treat cardiovascular disease. However, at least in the female heart, rapamycin may suppress the recruitment of putative signalling events conferring cardioprotection. The present study tested the hypothesis that rapamycin-sensitive signalling events contributed to the cardioprotective phenotype of the female rat heart after an ischemic insult. Rapamycin (1.5 mg/kg) was administered to adult female Sprague–Dawley rats 24 h after complete coronary artery ligation and continued for 6 days. Rapamycin abrogated p70S6K phosphorylation in the left ventricle of sham rats and the noninfarcted left ventricle (NILV) of 1-week postmyocardial-infarcted (MI) rats. Scar weight (MI 0.028 ± 0.006, MI+rapamycin 0.064 ± 0.004 g) and surface area (MI 0.37 ± 0.08, MI+rapamycin 0.74 ± 0.03 cm2) were significantly larger in rapamycin-treated post-MI rats. In the NILV of post-MI female rats, rapamycin inhibited the upregulation of eNOS. Furthermore, the increased expression of collagen and TGF-β3 mRNAs in the NILV were attenuated in rapamycin-treated post-MI rats, whereas scar healing was unaffected. The present study has demonstrated that rapamycin-sensitive signalling events were implicated in scar formation and reactive fibrosis. Rapamycin-mediated suppression of eNOS and TGF-β3 mRNA in post-MI female rats may have directly contributed to the larger infarct and attenuation of the reactive fibrotic response, respectively.


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