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Early protein restriction and obesity independently induce hypertension in 1-year-old rats
C J Petry1, S E Ozanne, C L Wang
1Clinical Biochemistry Department, University of Cambridge, Addenbrook's Hospital, U.K.
Insights
Early life protein restriction and later obesity independently increase hypertension risk. This study in rats shows these factors contribute to insulin resistance syndrome features, highlighting crucial developmental periods for metabolic health.
Area of Science:
- Metabolic Syndrome Research
- Developmental Programming
- Nutritional Epidemiology
Background:
- Fetal and early postnatal growth retardation, often linked to nutritional deficits, is associated with later-life insulin resistance syndrome.
- Obesity is a significant risk factor for developing features of the insulin resistance syndrome.
- Hypertension is a key component of the insulin resistance syndrome, and its developmental origins are of significant interest.
Purpose of the Study:
- To investigate whether maternal and early protein restriction, leading to growth retardation, and subsequent obesity are independent risk factors for developing features of the insulin resistance syndrome.
- Specifically, to determine the independent and combined effects of early protein restriction and later obesity on the development of hypertension.
- To assess the impact of these nutritional manipulations on glucose tolerance and lipid profiles.
Main Methods:
- Pregnant Sprague-Dawley rats were fed either a 20% or 8% protein isocaloric diet throughout gestation and lactation.
- Female offspring were weaned onto the same maternal diets and maintained until 70 days of age.
- Post-weaning, half the rats received standard chow, while the remainder were fed a cafeteria-style diet to induce obesity, with measurements taken at 1 year of age.
Main Results:
- Rats on the 8% protein diet exhibited sustained lower body weight compared to the 20% protein group.
- Cafeteria-fed rats showed significant weight gain and impaired glucose tolerance, along with hypertriacylglycerolaemia.
- Both early protein restriction (8% protein diet) and later cafeteria feeding independently increased systolic blood pressure, with additive effects observed.
Conclusions:
- Early life protein restriction and later-life obesity act as independent risk factors for the development of hypertension.
- These nutritional insults during critical developmental periods can program the offspring for features of the insulin resistance syndrome.
- The findings underscore the importance of maternal nutrition and early life diet in long-term metabolic health and cardiovascular risk.
Abstract:
1. Recent studies have revealed a link between fetal and early post-natal, growth retardation and the development of features of the insulin resistance syndrome in later life. Obesity is also a strong risk factor for this syndrome. The aim of this study was to assess whether maternal and early protein restriction, which causes growth retardation, and obesity are risk factors that are independent for the development of certain features of the insulin resistance syndrome, especially hypertension. 2. Pregnant Sprague-Dawley rats were given either 20% or 8% protein isocaloric diets throughout pregnancy and lactation. Female offspring were weaned onto the same diets as their mothers and they remained on these diets until 70 days of age. Half the rats were then given standard laboratory chow, whilst the remainder were fed a highly palatable cafeteria-style diet. Rats were maintained on these diets for the remainder of the study. 3. Rats given the 8% protein diet remained physically lighter than comparable animals fed the 20% protein diet throughout the study. In contrast, cafeteria-fed rats showed excessive weight gain. At 1 year of age the rats had their systolic blood pressures and fasting lipids measured, as well as undergoing an intraperitoneal glucose-tolerance test. 4. Cafeteria-fed rats had worse glucose tolerances than controls and hypertriacylglycerolaemia. The early 8% protein rats had significantly increased blood pressures, as did the cafeteria-fed rats. These increases were additive, suggesting that early protein restriction, and later obesity, are indeed independent risk factors for the development of hypertension.