Adverse effects of perinatal protein restriction on regulators of lipid metabolism and hepatic function in offspring of sprague-dawley rats

Abstract

Background: Adequate evidence suggests that a poor in utero environment produced by early-life dietary disturbance may predispose offspring to chronic diseases in later life. It remains to be defined which of the windows of early exposure due to perinatal protein restriction (PPR) (gestation, lactation, and/or both) is more detrimental to the regulators of lipid metabolism and hepatic functions of the offspring in later life. Hence, the current study investigated the role of PPR on regulators of lipid metabolism and hepatic functions in adult offspring. Materials and Methods: Twenty-four pregnant Sprague-Dawley rats were used and fed either a control (CONT) diet containing 20% protein or protein-restricted (PR) diet with 8% protein. The dams were given PR diet up to parturition (in utero group, in utero protein restriction [IUPR]), or from birth to postnatal day (PND) 21 (lactation group, lactational protein restriction [LPR]) or for a period covering both (combined protein restriction [CPR]). On PND 126, triglycerides (TG), cholesterol (CHOL), low density lipoprotein (LDL), and high density lipoprotein (HDL) were determined and Castelli indices I and II were calculated. Hepatic lipase (HL) and lipoprotein lipase (LPL), aspartate aminotransferase (AST), alanine amino transferase (ALT), alkaline phosphatase (ALP), and serum albumin were also assessed. Results: There was a significant decrease (P < 0.01) in HDL with a significant increase (P < 0.01) in TG and LDL in IUPR and CPR offspring compared with CONT. The Castelli index I was significantly increased (P < 0.01) in all PR offspring with a significant increase (P < 0.01) in Castelli index II in LPR offspring compared with CONT. HL and LPL activities reduced significantly (P < 0.01) in all PR offspring. PPR produced a significant reduction (P < 0.01) in AST with a significant elevation in ALT in all PR, while ALT heightened significantly (P < 0.01) in CPR offspring. A significant decrease (P < 0.01) was observed in albumin level in CPR offspring compared with CONT. Conclusion: In conclusion, it is evidenced that PPR at critical periods of early-life exposure blunted remarkably the actions of HL and LPL which consequently led to impairment of lipid metabolism and hepatic dysfunction.