Fish oil n-3 fatty acids selectively limit the hypertrophy of abdominal fat depots in growing rats fed high-fat diets

• Published in: The American journal of physiology Vol. 264; no. 6; p. R1111
• Main Authors: Belzung, F, Raclot, T, Groscolas, R
• Format: Journal Article
• Language: English
• Published: United States 01.06.1993
• Subjects: ABDOMEN; ACEITES DE PESCADO; ACIDE GRAS POLYINSATURE; ACIDOS GRASOS POLIINSATURADOS; Adipose Tissue - metabolism; Adipose Tissue - pathology; Aging - physiology; Animals; Body Weight - drug effects; CELLULE; CELULAS; CORPS GRAS; DIETA; Dietary Fats - pharmacology; DIGESTIBILIDAD; DIGESTIBILITE; Energy Intake; Fatty Acids - urine; Fatty Acids, Omega-3 - pharmacology; Fish Oils - pharmacology; Food; GRASAS; HIPERTROFIA; HUILE DE POISSON; HYPERTROPHIE; Hypertrophy; LIPEMIA; LIPEMIE; Lipid Metabolism; Male; METABOLISME DES LIPIDES; METABOLISMO DE LIPIDOS; RAT; RATA; Rats; Rats, Wistar; Reference Values; REGIME ALIMENTAIRE; SOBREPESO; SURPOIDS; TEJIDO ADIPOSO; TISSU ADIPEUX; TRIGLICERIDOS; TRIGLYCERIDE; Triglycerides - blood
• ISSN: 0002-9513; 2163-5773
• DOI: 10.1152/ajpregu.1993.264.6.r1111

Because dietary n-3 polyunsaturated fatty acids (n-3 PUFA) from fish oils have profound effects on lipid metabolism, we examined whether they influence the growth of adipose tissue at different locations in growing rats. Rats were fed for 4 wk on high-fat (HF) diets (20% fat) containing very low (L), medium (M), and high (H) amounts of n-3 PUFA but similar amounts of saturated fatty acids and n-6 PUFA. A fourth group was fed a standard laboratory diet (control group) to estimate changes in adipose tissue mass related to growth. At the end of the dietary treatment, the lipid mass (LM) of the four major adipose depots (subcutaneous, SC; mesenteric, MES; retroperitoneal, RP; epididymal, EPI) and total adiposity were significantly higher in each of the three HF groups than in the control group. The lipid gain in EPI was due to fat cell hypertrophy alone, whereas RP showed both hypertrophy and hyperplasia. Energy intake, fatty acid excretion, and body mass were the same in the three groups fed HF diets. Similarly, there was no difference in the LM or in lipid gains specifically caused by HF feeding of SC and MES between the HF groups. In contrast, the LM of RP was significantly lower in the H than in the L and M groups (50 and 30%, respectively). The LM of EPI was also 30% lower in the H than in the L group. The lipid gains specifically caused by HF feeding were 2.5- and 5-fold lower in the H than in the M and L groups, respectively, for RP and 2-fold lower in the H than in the L group for EPI. Lower RP and EPI LM in the H and, to a lesser extent, M groups were related to reduced hypertrophy, since fat cell numbers were the same. RP hyperplasia induced by HF feeding was maintained in rats fed the H diet. Plasma triglycerides were markedly depressed in rats fed the H and M diets compared with the L group, and they correlated positively with the fat cell size in RP and EPI. In growing rats fed HF diets, n-3 PUFA from fish oils limit the hypertrophy of two abdominal adipose