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* Department of Diabetes-INSERM U341, Hôtel-Dieu Hospital, 75004 Paris, France;
INSERM U465, Institut Biomédical des Cordeliers, 75006 Paris, France; and
** Laboratory of Biochemistry, Hôtel-Dieu Hospital, 75004 Paris, France
3To whom correspondence should be addressed. E-mail: salwa.rizkalla{at}htd.ap-hop-paris.fr.
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ABSTRACT |
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 TOP ABSTRACT MATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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KEY WORDS: • (n-3) PUFA • fatty acid synthase • lipoprotein lipase • lipolysis • insulin-resistant rats
The beneficial effects of dietary fish oil (n-3) PUFA on insulin action in a variety of insulin-resistant rats fed high fat (1,2) or sucrose (3–5) are well documented.
In rats fed high fat, the amount and type of dietary fats have been shown to affect the development of fat depots in a site-dependent manner (6). Hypertrophy of perirenal and epididymal adipose tissues (Epi-AT) was lower in rats fed a fish oil diet than in those fed diets containing lard or beef tallow (7–9). Subcutaneous and mesenteric adipose tissues, however, were not affected by different fatty acids in the diet. In the sucrose-fed rats, fish oil in the diet also reduced the hypertrophy of visceral fat stores (Epi-AT) and retroperitoneal adipose tissues (Retro-AT) (3). The effect on subcutaneous adipose tissue (SCAT), however, was not evaluated. Moreover, mechanisms underlying the reduction of body fat stores by fish oil have not been demonstrated in sucrose-fed rats. Possible mechanisms include a reduction in the function and/or activity of some lipid storage–related enzymes such as fatty acid synthase (FAS) or lipoprotein lipase (LPL) in adipose tissue. The mobilization and loss of body fat by lipolysis might be another pathway.
In this study, therefore, our goal was to determine whether the presence of fish oil in the diet of insulin-resistant, sucrose-fed rats induces a site-specific regulation of body fat. We evaluated the effects of fish oil feeding on the activity of some lipid storage–related enzymes (FAS, LPL) as well as on lipolysis in isolated adipocytes in vitro.
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MATERIALS AND METHODS |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Male Sprague-Dawley rats (n = 24; Centre d’élevage R. Janvier, Le Genest-Saint-isle, France), 3 wk old, were housed in polypropylene cages (n = 4/cage) and maintained at 24°C with a 12-h light:dark cycle. Rats were initially fed a standard laboratory diet and had free access to food and water. After a 2-wk acclimation period, rats (210 ± 5 g body weight) were randomly assigned for 3 wk to one of two semisynthetic powder diets (INRA, Jouy-en-Josas, France) containing (g/kg) 575 sucrose, 210 protein and 140 fat, as either fish oil (SF), or a mixture of oils of vegetable and animal origins (SC) (10). Fish oil (MAXEPA) was donated by Pierre Fabre Medicaments Laboratory, Castres, France. Another group of rats, the reference group (R), was fed a standard powdered commercial diet (semipurified diet # 210, INRA) containing (g/kg diet) 575 g carbohydrates, 230 g protein and 55 g lipids (corn oil, 11; peanut oil, 11; lard, 33). Other constituents of the reference diets were 10 g/kg vitamin mixture, 70 g/kg minerals and 60 g/kg cellulose as described previously (11). Daily food intake was determined by weighing the food remaining in the cage. Rats were weighed once each week. At the end of the experimental period, fed rats were decapitated between 0830 and 0930 h. Food was withdrawn 1 h before decapitation. Blood was collected and plasma immediately separated by centrifugation (10 min at 900 x g) and stored at -20°C until plasma lipids and leptin concentrations were determined. Liver, muscle, and epididymal, subcutaneous and retroperitoneal fat pads were removed, weighed, rapidly minced and immediately frozen in liquid nitrogen and stored at -80°C. A portion of the fresh epididymal adipose tissue was used immediately to measure lipolysis in vitro.
Because the decapitation and the measurements of plasma metabolites took place in fed rats, and the fed state might influence plasma glucose and insulin levels, these variables were examined in rats that had been food-deprived 3 d before decapitation. Rats were deprived of food at 0800 h for 6 h. At 1430 h, rats were anesthetized with a small dose of pentobarbital and blood samples were taken from the tip of the tail.
Approval to use laboratory animals was given by the French Ministry of Agriculture and the protocol complied with the NIH guidelines for the care and use of laboratory animals.
Preparation of isolated fat cells.
Fat cells were isolated from the epididymal adipose tissue as described by Rodbell (12). Minced epididymal fat pads were incubated with crude collagenase (2 mg/g tissue: Type II, Sigma, St. Louis, MO) at 37°C for 60 min in Krebs-Ringer bicarbonate buffer (pH 7.4) containing 35 g/L bovine serum albumin (BSA; Sigma RIA grade) and 1 g/L D-glucose. Isolated fat cells were filtered through a 250-µm nylon screen and washed three times with collagenase-free buffer and then diluted with three volumes of buffer.
Lipolysis experiments.
Aliquots of 100 µL were incubated in triplicate at a final concentration of 2% (v/v) for 60 min at 37°C in the presence or absence of isoprenaline (Isuprel, Winthrop Laboratory, Ambares, France) at concentrations of 10-8 to 10-5 mol/L. The final incubation volume was 500 µL. The reaction was stopped at 0°C after 60 min. Glycerol released by adipocytes into the incubation medium was taken as an index of lipolysis rate (13) and measured by the Enzymatic Bio-Analysis-Food kit (Boehringer, Mannheim, Germany). Various amounts of glycerol were corrected by the quantity of total lipids determined by the Dole method (14).
FAS activity.
Adipose tissues and the liver were homogenized in ice-cold buffer containing 0.25 mol/L sucrose, 1 mmol/L dithiothreitol, 1 mmol/L EDTA and 0.1 mol/L phenylmethylsulfonyl fluoride, pH 7.4; cytosolic fractions were obtained by centrifugation (1 h, 105000 x g at 4°C). Infranatants (below the fat cake) were immediately used for spectrophotometric assay of FAS (EC 2.3.1.85) by measuring malonyl-CoA–dependent oxidation of NADPH at 37°C, according to the Halestrap method (15). One unit of enzyme activity represents the oxidation of 1 nmol NADPH/min at 37°C. Protein concentration was measured using BSA as the standard (16).
LPL activity.
Muscle and adipose tissue were homogenized in ice-cold 0.15 mol/L NaCl containing 4 g/L BSA as the carrier protein and heparin (2000 U/L). Acetone/diethyl ether–dried powders were prepared and suspended in 5 mmol/L sodium veronal buffer, as described previously (17). LPL (EC 3.1.1.34) activity was measured in the clear supernatant obtained after centrifugation of the suspension (3000 x g for 15 min at 4°C) with a [14C] trioleylglycerol emulsion made in glycerol, as previously described (17). The same emulsion was used throughout the study. Heat-inactivated serum was added as a source of apolipoprotein CII. The reaction was stopped by the successive addition of CH3OH/CHCl3/heptane (1.41:1.25:1, v/v/v) and 0.1 mol/L sodium potassium tetraborate buffer, pH 10.5. 14C radioactivity was determined in 1.5-mL aliquots of the upper phase. One unit of LPL activity represents 1 µmol of fatty acids released per hour at 37°C.
Plasma assays.
Plasma glucose was measured by the glucose oxidase method (Glucose Analyzer II, Beckman, Fullerton, CA) and plasma insulin by RIA (Bi-insulin RIA Diagnostic, Pasteur, Paris, France). Plasma triacylglycerols (Triglycerides Enzymatiques kits, BioMérieux, Marcy-l’Etoile, France), plasma cholesterol (Labintest Cholesterol kits, Labintest, Aix-en-Provence, France), free fatty acids (NEFA C kit, Unipath, Dardilly, France) and leptin (Linco’s Rat Leptin RIA kit, Clinisciences, Montrouge, France) concentrations were determined.
Statistical analysis.
All comparisons were done by a one-way ANOVA followed by Fisher’s Least Significant Difference post-hoc test. A first comparison was made between the SC-fed rats and the R group to characterize the sucrose-fed rats, and then the two experimental groups (SC, SF) were compared. All analyses were carried out with Statview 512+ software program (Brainpower, Calabasas CA). Results are given as means ± SEM. Differences were considered significant when P < 0.05.
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RESULTS |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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At the end of the 3 wk, sucrose-fed rats had lower food intake than R rats (P < 0.005), but similar energy intake. Body weights, and relative liver and adipose tissue weights did not differ between the SC and in the R groups (Table 1). The SC-fed rats had slightly greater plasma glucose levels (P < 0.001) but 100% greater plasma insulin levels (P < 0.05) and twofold greater plasma triacylglycerol (P < 0.0005) and free fatty acid concentrations (P < 0.001). These modifications in the SC group were associated with higher plasma glycerol (P < 0.01) and leptin (P < 0.005) concentrationss than in the R rats. In adipose tissue, however, lipid storage–related enzyme activities of the SC-fed rats were similar to those in the R rats (Table 2). In the liver, FAS activity was higher in the SC-fed rats than in the R rats (P < 0.01).
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Food intake, body and tissue weights. Body weight, food and energy intakes did not differ between the SC and SF groups (Table 1). However, the relative epididymal (P < 0.01) and retroperitoneal (P < 0.05) fat pad weights were lower in the SF group than in the SC group.
Plasma variables. Plasma glucose and insulin in food-deprived rats were lower in the SF than in the SC group (P < 0.05). In rats fed the SF diet, plasma triacylglycerol was lowered by 80% (P < 0.0005), cholesterol by 38% (P < 0.01) and free fatty acids by 52% (P < 0.05) compared with the SC group. Plasma glycerol did not differ between groups. After 3 wk, plasma leptin levels in rats consuming the SF diet were 26% (P < 0.005) greater than those in the SC group. The present data confirm and extend previous results from our laboratory (3).
Isoprenaline stimulated lipolysis. Basal lipolysis did not differ in the two experimental groups (Figure 1). The dose-response curves for isoprenaline-stimulated lipolysis, however, revealed that the quantity of glycerol released from adipocytes of the fish oil–fed rats was significantly higher than that in the SC group at all isoprenaline concentrations. Maximal lipolytic responses were reached at an isoprenaline concentration of 10-6 mol/L in cells from both groups. The maximal biological effect (glycerol released at 10-6 mol/L isoprenaline minus basal values) was higher in the SF than in the SC group (P < 0.05).
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LPL activity. In adipose tissue, LPL activity was one- to twofold greater in the Epi-AT, Retro-AT (both P < 0.005) and SCAT (P < 0.01) of the SF-fed rats than in those of the SC-fed rats. In muscle, however, LPL activity did not differ between the two groups (Table 2).
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DISCUSSION |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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There is now clear evidence that the nature of the dietary fat can influence overall lipid metabolism such as plasma lipid profile and body fat deposition. The mechanisms leading to the decrease in visceral adipose tissue after fish oil consumption may play a role here. Fatty acid synthase (FAS), one of the major key lipogenic enzymes that control the lipogenic capacities of both liver and adipose tissue, also might play a role. In the present study, FAS activity was regulated in a tissue-specific manner. Indeed, in the liver, the fish oil in the sucrose diet prevented the increase in hepatic FAS activity found in the SC-fed, insulin-resistant rats. This finding is in full agreement with previous studies in other models (18,19) and may contribute to the hypolipidemic effect of dietary fish oil. However, changes in adipose tissue FAS activity, in the present study, paralleled changes in plasma triacylglycerol concentrations. Both were increased by sucrose feeding and lowered by fish oil supplementation. These results are consistent with those of Goodridge et al. (20) who demonstrated in rats that a high carbohydrate diet increases FAS activity and lipogenesis in the liver. In adipose tissue, however, this regulation was the opposite, i.e., FAS activity was similar or higher in SF-fed rats than in the SC-fed rats, whereas triacylglycerol levels were lower in the SF-fed rats than in the SC-fed rats. It has been found that adipose tissue lipogenesis was inversely correlated with hepatic lipogenesis, assessed either by measuring mRNA levels of FAS (21) or by the use of stable isotopes in vivo (22). Recently, Diraison et al. (23) demonstrated that in obese subjects, the lipogenic capacity of adipose tissue appeared to decrease with lower FAS mRNA levels than in nonobese subjects. The same authors suggested that hepatic lipogenesis could contribute to the regulation of fat mass, but no evidence exists to support the contribution of the lipogenic capacity of adipose tissue. These results suggest that the regulation of FAS mRNA or activity in adipose tissue may depend on substrate availability rather than on plasma hormonal concentrations, and thus may differ from hepatic regulation. It has been suggested also that adipose tissue FAS levels are constitutively high unless suppressed by exogenous substrate availability. This reciprocal regulation of the lipogenic capacity of liver and adipose tissue was found also under other dietary conditions in rats (22,24–26).
The surprising increase in FAS activity in adipose tissue of SF-fed rats could not explain the low epididymal and retroperitoneal adipose tissue weights in these rats. An alternative mechanism might be a decrease in both plasma triglyceride hydrolysis and fatty acid uptake in adipose tissue through a negative regulation of LPL activity. Fish oil feeding in the present study, however, increased LPL activity in all adipose tissues studied, both visceral and subcutaneous, relative to SC-fed rats. Muscle LPL activity, on the other hand, was not affected by dietary fish oil. The increased adipose tissue LPL activity could be related to the increased adipose tissue insulin sensitivity in rats fed fish oil. Indeed, fish oil consumption prevents sucrose-induced insulin resistance in adipose tissue (3) and thus might indirectly mediate the regulation of LPL activity. The fact that muscle LPL did not change means that it is likely not related to the lower plasma triacylglycerol levels. Thus, triacylglycerol clearance, in this rat model is more likely related to adipose tissue LPL. However, this increase in adipose tissue LPL activity could not explain the reduction in visceral fat hypertrophy in rats fed fish oil.
Increased fatty acid mobilization from adipose tissue by lipolysis could be another explanation for the reduction in visceral adipose weight in rats fed fish oil. This is likely because in the present study, stimulated lipolysis in vitro was greater in adipocytes of SF- than in those of SC-fed rats. These results are consistent with those of Rustan et al. (27) who found that dietary (n-3) fatty acids increased total lipolysis in mesenteric and subcutaneous fat cells compared with adipocytes derived from lard-fed animals. In the present study, however, lipolysis was measured only in epididymal adipocytes. Increased lipolysis in fish oil–fed rats is in agreement with the fact that the enrichment of adipose tissue in specific long-chain highly unsaturated fatty acids such as eicosapentaenoic (EPA) and docosahexaenoic acids increases their selective mobilization in vitro (28). This hypothesis is strengthened also by the finding that the fatty acid composition of adipose tissue triacylglycerols largely reflects, but is not identical to that of the diet (29,30). The proportion of (n-3) PUFA in adipose tissue was lower than that of the diet (29). The preferential release of some highly unsaturated fatty acids such as (n-3) PUFA can explain in part their low proportion in adipose tissue triacylglycerols compared with the diet (31). Raclot and Groscolas (32) demonstrated that dietary essential (n-3) PUFA are selectively mobilized from fat stores. The preferential mobilization of EPA could contribute to this increase in lipolysis. Together, these data suggest that the part of adipose tissue formed mainly of (n-3) PUFA will be rapidly mobilized in vivo and thus reduced. Recently, Soria et al. (33), using a somewhat different experimental design, demonstrated that after the insulin resistance was induced by 90 d of sucrose feeding, fish oil in the diet only normalized the isoprenaline-stimulated lipolysis, but did not increase it as in the present study. These differences might be due to the different lengths of the diet periods and or the time of the introduction of fish oil into the sucrose diet (before or after the induction of insulin resistance). Caution is warranted, however, when studying individual adipose depots because heterogeneity among adipose tissue depots makes it difficult to extrapolate the results to whole-body lipolysis.
Increased lipolysis from consumption of dietary fish oil is not the only pathway that limits adipose tissue hypertrophy. Increased lipid oxidation at the expense of storage (34) as well as the contribution of increased energy expenditure might be additional factors contributing to the reduction in adipose tissue mass that require close examination. Moreover, recent studies demonstrated that (n-3) PUFA limit the development of visceral adipose tissue by suppressing the late phase of adipocyte differentiation through modifications of peroxisome proliferator-activated receptor 
(35).
Thus, changes in FAS and LPL activities did not contribute to the reduction of visceral adipose tissue mass after 3 wk of fish oil feeding. However, increased lipolysis due to fish oil feeding might explain part of this reduction. The increased and sustained high LPL activity in all adipose tissues studied is a mechanism in addition to decreased hepatic FAS activity that reduces circulating triacylglycerol levels.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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2 Supported by a grant from the National Institute of Health and Medical Research (INSERM) and by Pierre and Marie Curie University.
4 Abbreviations used: BSA, bovine serum albumin; EPA, eicosapentaenoic acid; Epi-AT, epididymal adipose tissue; FAS, fatty acid synthase; LPL, lipoprotein lipase; R, reference group; Retro-AT, retroperitoneal adipose tissue; SC, sucrose-control oil group; SCAT, subcutaneous adipose tissue; SF, sucrose-fish oil group.
Manuscript received 5 December 2002. Initial review completed 10 January 2003. Revision accepted 11 February 2003.
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LITERATURE CITED |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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