A Perinatal Palatable High-Fat Diet Increases Food Intake and Promotes Hypercholesterolemia in Adult Rats
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- Oliveira, T.W.S., Leandro, C.G., de Jesus Deiró, T.C.B. et al. Lipids (2011) 46: 1071. doi:10.1007/s11745-011-3604-7
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The main goal of the present study was to evaluate the long-term effects of a perinatal palatable high-fat diet on the food intake and cholesterol profile of adult rats. Male Wistar rats (aged 22 days) were divided into two groups according to their mother’s diet during gestation and lactation (Cp, n = 10; pups from control mothers; and HLpn = 10; pups from mothers fed a palatable high-fat diet). At the 76th day, pups were housed individually for 14 days, and daily food consumption was determined during a period of 6 days. Blood from 100-day-old rats was sampled by cardiac puncture. Fasting (12 h) serum glucose, total cholesterol, LDL-C, HDL-C, triglycerides (TG), and VLDL-C levels were determined. The measurement of food intake was higher in the animals submitted to a hyperlipidic diet during the perinatal period. Serum total cholesterol, LDL-C, HDL-C, TG, VLDL-C and glycemia were increased in the HLp group compared to the control group. Our findings show that an early life environment with a high-fat diet can contribute to metabolic disease in later life.
KeywordsHyperlipidic dietCholesterolemiaRatsDevelopmental plasticityCritical period of development
Hyperlipid diet pups
Monounsaturated fatty acids
Polyunsaturated fatty acids
Saturated fatty acids
Trans fatty acids
The etiology of metabolic syndrome has been associated with the perinatal environment, according to previous evidence from experimental studies and epidemiological research [1–3]. Developmental plasticity is the term used to explain the events operating at a critical or susceptible period of development and the lasting consequences for the structure or function of the organism . Our previous studies using rats demonstrated that postnatal undernourishment (multi-deficient diet with 7% protein) may influence brain growth spurt, feeding behavior, ontogeny of reflexes, skeletal muscle mechanical properties and locomotor activity in adult rats [5–7].
Developmental plasticity is now observed when an organism is exposed to very high caloric nutrition before birth . In fact, human studies have shown that high-fat diet availability during gestation and lactation, as well as gestational diabetes, may predispose offspring to increased fat mass and incidence of metabolic syndrome as children and adults . In animals, maternal high fat or cholesterol over-feeding during the perinatal period is associated with long-lasting effects on the offspring such as: dyslipidemia, hyperleptinemia, increased adiposity and blood pressure, elevated blood glucose and triglycerides [9, 10]. Litter size reduction (3 pups/litter) resulted in postnatal overfeeding during the suckling period and elevated blood pressure in adulthood . Previous studies have related early adiposity to faster growth and hyperphagia (suppressed orexigenic signals), as seen in 20-postnatal-day offspring from mothers submitted to a high-fat diet during gestation . Out of this context, the main goal of the present study is to evaluate the long-term effects of a palatable high-fat diet during gestation and lactation on the food intake and lipids profiles of offspring.
Materials and Methods
Animals and Diet
Analysis of fatty acid percentage composition of the diets
Ingredients (g/100 g)
Individual fatty acids (g/100 g of total fatty acid)
Total fatty acids
Total MUFA cis
Total PUFA cis
Measurement of Food Intake and Fasting Serum Glycemia and Cholesterol Profile
On day 76, pups were housed individually for 14 days in a metabolic cage. The first 4 days were designed for adaptation to the cage. Next, the animal’s daily food consumption was determined by the difference between the amount of food provided (50 g) at the onset of the light cycle and the amount of food remaining 24 h later. Body and food weights were recorded by a Marte Scale (AS-1000), in increments of 0.01 g . At 100 days old, and after fasting (12 h), serum glucose, total cholesterol, high-density-lipoprotein cholesterol (HDL-C) and triglyceride (TG) levels were determined with commercially available kits (BioSystems, Spain—A 25 Clinical Chemistry Analyse®). Low-density-lipoprotein cholesterol (LDL-C) and very low-density-lipoprotein cholesterol (VLDL-C) were obtained using Friedwald calculations .
Results are presented as means ± standard errors of the mean. Data for all analyses were performed using the statistical program Graphpad Prism 5® (GraphPad Software Inc., La Jolla, CA, USA). For statistical analysis of body weight and food intake, a two-way repeated measures ANOVA was used, with the mother’s diet (HL) and time (weeks) as factors. Bonferroni’s post hoc test was used, and Student’s t test was used to compare groups in terms of blood biochemical parameters. Significance was set at P < 0.05.
Results and Discussion
The measurement of food intake during a period of 6 days was higher in the HLp group (Fig. 1b). High food intake can be associated with a high adiposity, high leptinemia and leptin resistance . There is a correlation between high leptin resistance and the relative food intake per gram of body weight . Although the concentrations of leptin were not evaluated in the present study, previous studies have found that a perinatal high-fat diet or gestational diabetes can lead to hyperinsulinism and a malprogramming in central regulators of body weight and metabolism .
Fasting serum glycemia and cholesterol profile of pups at 90 days old from mothers submitted to either a control or a hyperlipidic diet during gestation and lactation
Total cholesterol (mg/dL)
35.1 ± 1.0
56.4 ± 3.3*
9.6 ± 1.1
19.14 ± 2.2*
16.6 ± 0.7
25.5 ± 1.3*
44.2 ± 4.1
58.8 ± 5.5*
8.84 ± 0.8
11.76 ± 1.1*
171.6 ± 11.1
217 ± 10.6*
Perinatal nutrition-induced hypercholesterolemia has been previously described in animal models, and the offspring’s susceptibility to programmed obesity risk has been shown to be dependent on the timing and severity of diet manipulation . Most models have used malnutrition as a stimulus for developmental plasticity, and relatively few studies have seen the effects of a high-fat diet during gestation and lactation. In this regard, we have presented data that confirm our hypothesis by demonstrating that a palatable high-fat diet during perinatal period increases food intake and induces hypercholesterolemia. In conclusion, our observations extend the evidence that both gestation and lactation are critical periods for the development of metabolic disease in later life.
This study received financial support from the CNPq and FAPESB.