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Fat Preference: A Novel Model of Eating Behavior in Rats
Published on: June 27, 2014
Prenatal exposure to undernutrition and programming of responses to high-fat feeding in the rat
Aml Erhuma1, Leanne Bellinger, Simon C Langley-Evans
1School of Biomedical Sciences, University of Nottingham, Queens Medical Centre, Nottingham NG7 2UH, UK.
Insights
Prenatal low-protein (LP) diet can program offspring for metabolic disorders. A high-fat (HF) diet post-birth alters fat deposition and gene expression, particularly in females, highlighting the interaction of early nutrition and later diet.
Area of Science:
- Developmental biology
- Nutritional science
- Metabolic research
Background:
- Fetal undernutrition is linked to later metabolic disorders.
- Postnatal environmental factors can modify these programmed risks.
- Understanding these interactions is crucial for preventing metabolic diseases.
Purpose of the Study:
- To investigate the impact of a postnatal high-fat (HF) diet on body weight, adiposity, and gene expression in offspring exposed to prenatal low-protein (LP) undernutrition.
- To determine how the timing of LP exposure during gestation influences these outcomes.
- To explore the interplay between prenatal nutrition, postnatal diet, sex, and age in metabolic programming.
Main Methods:
- Pregnant rats were fed control or LP diets during specific gestational periods (LPE, LPM, LPL).
- Offspring were fed either a standard chow or HF diet from 12 to 22 weeks of age.
- Body weight, abdominal fat, and gene expression (galanin, galanin-2 receptor, SREBP-1c) in the hypothalamus and liver were analyzed.
Main Results:
- Prenatal LP exposure did not affect overall weight gain or abdominal fat in males on a HF diet.
- Females exposed to LP in utero showed similar weight gain on HF and chow diets.
- Fat deposition programming occurred in LPE females and LPM/LPL males (P = 0.019).
- Hypothalamic galanin-2 receptor expression was altered by LP in female offspring.
- Hepatic SREBP-1c expression (mRNA and protein) was decreased by LP, and HF feeding response was blunted in LP groups.
Conclusions:
- Prenatal undernutrition programs offspring for altered fat deposition and metabolic gene expression.
- Postnatal diet, particularly HF feeding, interacts with prenatal LP exposure to influence metabolic outcomes.
- The timing of prenatal LP exposure and offspring sex are critical factors in determining metabolic programming and responsiveness.
- This study confirms the role of prenatal nutrition in programming genes related to lipid metabolism and appetite regulation.
Abstract:
Fetal undernutrition programmes risk of later metabolic disorders. Postnatal factors modify the programmed phenotype. This study aimed to assess the effects of a postnatal high-fat (HF) challenge on body weight gain, adiposity and gene expression following prenatal undernutrition. Pregnant rats were fed either a control diet or a low-protein (LP) diet, targeted at days 0-7 (LPE), days 8-14 (LPM), or days 15-22 (LPL) gestation. At 12 weeks of age offspring were either fed standard laboratory chow diet (4.13 % fat), or a 39.5 % fat diet, for 10 weeks. LP exposure had no effect on weight gain or abdominal fat in males. Females exposed to LP diet in utero exhibited a similar weight gain on HF diet as on the chow diet. Programming of fat deposition was noted in LPE females and males of the LPM and LPL groups (P = 0.019). Hypothalamic expression of galanin mRNA was similar in all groups, but expression of the galanin-2 receptor was modified by LP exposure in female offspring. Hepatic expression of sterol response element binding protein (SREBP-1c) was decreased by LP at both the mRNA (P = 0.008) and protein (P < 0.001) level. HF feeding increased expression of SREBP-1c mRNA three-fold in controls, with little response noted in the LP groups. Interactions of factors such as postnatal diet, age and sex act together with prenatal factors to determine metabolic function and responsiveness at any stage of postnatal life. This study further establishes a role for prenatal nutrition in programming the genes involved in lipid metabolism and appetite regulation.
