Epidemiological and animal studies suggest that the alteration of hormonal and metabolic environment during fetal and neonatal development can contribute to development of metabolic syndrome in adulthood. In this paper, we investigated the impact of maternal high-fat (HF) diet on hypothalamic leptin sensitivity and body weight gain of offspring. Adult Wistar female rats received a HF or a control normal-fat (C) diet for 6 wk before gestation until the end of the suckling period. After weaning, pups received either C or HF diet during 6 wk. Body weight gain and metabolic and endocrine parameters were measured in the eight groups of rats formed according to a postweaning diet, maternal diet, and gender. To evaluate hypothalamic leptin sensitivity in each group, STAT-3 phosphorylation was measured in response to leptin or saline intraperitoneal bolus. Pups exhibited similar body weights at birth, but at weaning, those born to HF dams weighed significantly less (−12%) than those born to C dams. When given the HF diet, males and females born to HF dams exhibited smaller body weight and feed efficiency than those born to C dams, suggesting increased energy expenditure programmed by the maternal HF diet. Thus, maternal HF feeding could be protective against adverse effects of the HF diet as observed in male offspring of control dams: overweight (+17%) with hyperleptinemia and hyperinsulinemia. Furthermore, offspring of HF dams fed either C or HF diet exhibited an alteration in hypothalamic leptin-dependent STAT-3 phosphorylation. We conclude that maternal high-fat diet programs a hypothalamic leptin resistance in offspring, which, however, fails to increase the body weight gain until adulthood.

in several animal models, including hamsters, but the mechanism of action of the main food-derived CLA isomer is unknown in this species. This study thus focused on cis-9,trans-11-CLA (rumenic acid), and its effect was compared with that of fish oil, which is known to influence several aspects of atherogenesis. Syrian hamsters were fed (for 12 wk) diets containing 20% (wt/wt) butter fat (B diet) or the same diet augmented with either 1% (wt/wt) of a cis-9,trans-11-CLArich oil (BR diet) or 1% (wt/wt) fish oil (BF diet). The BR diet induced the lowest aortic lipid deposition (from Ϫ30% to Ϫ45%) among the butter oil-fed hamsters. In this group, plasma also displayed a reduced non-HDL-to-HDL-cholesterol ratio (21% less than in the butter oil group) and inflammatory serum amyloid A levels (70 -80%) and an improvement of anti-oxidized LDL paraoxonase activity (all P Ͻ 0.05). Compared with the B group, the beneficial effects of the BR diet could be further explained in part by preventing the high VCAM-1 expression rate, increasing (30%) ATP-binding cassette subfamily A1 expression in the aorta, and downregulating expression of inflammatory-related genes (TNF-␣, IL-1␤, and cyclooxygenase 2, 2-to 2.8-fold, P Ͻ 0.05). This effect was partly associated with an activation of peroxisome proliferator-activating receptor (PPAR)/liver X receptor (LXR)-␣ signaling cascade. Interestingly, activation of PPAR/LXR-␣ signaling was not observed in hamsters fed the BF diet, in which the early signs of atherogenesis were increased. In conclusion, this study demonstrated that milk fat-rich cis-9,trans-11-CLA reduces the atherogenic process in hyperlipidemic hamsters.

Milk fat is usually considered to be proatherogenic, although its fatty acid composition can vary, due mainly to farming conditions. No study has evaluated whether such variation can modify the atherogenic properties of dairy fat. Aortic lipid deposition and related risk factors were examined in Syrian hamsters fed diets for 12 wk containing 200 g/kg of 2 commercial milk fats [high content of saturated fatty acids (HSF) and low content of saturated fatty acids (LSF)] contrasting, respectively, in total saturated fatty acids (72 vs. 67 g/100 g), 18:1, trans (4.24 vs. 7.26 g/100g), and conjugated linoleic acid (mainly cis-9,trans-11 or rumenic acid; 0.39 vs. 2.59 g/100 g). Hamsters fed the LSF-diet had 25% less aortic cholesteryl-ester deposition than those fed the HSF-diet; this was accompanied by an improved plasma cholesterol profile (lower LDL cholesterol and LDL:HDL cholesterol ratio), a lower local inflammatory status (aortic gene expression of cyclooxygenase-2), and lower aortic gene expression of vascular cell adhesion molecule-1 (all P < 0.05). Supplementation of the LSF-diet with rumenic acid (up to 9 g/kg) amplified the antiatherogenic effect of the original LSF-diet compared with the HSF-diet, i.e., less aortic cholesterol loading, increased reverse cholesterol transport potential (higher plasma HDL cholesterol concentration and ATP-binding cassette, subfamily A, transporter 1 gene expression in aorta), and decreased LDL-peroxidability index and gene expression of proinflammatory IL-1beta in the aorta (all P < 0.05). In conclusion, our results suggest that the atherogenic potential of milk fat can be greatly reduced in products with a naturally high abundance of rumenic acid, and argue for increasing this fatty acid in milk.

We examined the effects of feeding conjugated linoleic acids (CLA) to adult male hamsters on several components of energy metabolism and body composition. Hamsters (n = 54) were assigned for 6-8 wk to one of three diets: 1) a standard diet (in percentage energy: lipids, 33, carbohydrates, 49, and proteins, 18); 2) to the standard diet augmented with the 9c,11t-isomer of CLA to 1.6% of energy (R group); or 3) the standard diet augmented with the 9c,11t-isomer and the 10t,12c-CLA isomer to 3.2 (1.6 + 1.6) % of energy (CLA mix group). (15)N uniformly labeled milk-protein was included in the diet to measure the incorporation of dietary protein into liver and muscle. Basal metabolic rate, thermogenic response to feeding and energy expenditure during spontaneous activity or during an exercise at approximately 60% of VO(2max) were measured. Carnitine palmitoyltransferase-I (CPT-I), leptin, insulin and triiodothyronine concentrations, as well as the in vivo overall adiposity changes were also determined. After 6 wk, the whole-body triglyceride content determined in vivo by NMR was significantly higher in the R group than in the control and CLA mix groups. The CLA mix group differed from the others in the lack of body triglyceride accumulation between d 21 and d 45 of the study, and the appearance of a slight insulin-resistance (homeostatic model assessment index, P < 0.05). Paradoxically, the lack of effect on whole-body lipid oxidation was associated with a greater CPT-I-specific activity in tissues of both CLA-fed groups (P < 0.05). No other major effects of CLA feeding were detected. In conclusion, CLA supplementation in hamsters did not affect adipose weight or the components of energy expenditure despite a theoretically higher capacity of red muscle to oxidize lipids. Only a CLA mixture prevented whole-body triglyceride accumulation over time.

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