MATERNAL HIGH‑MONOSACCHARIDE DIETS CHANGE BEHAVIOR AND MELANOCORTIN TYPE 4 RECEPTORS EXPRESSION IN RAT OFFSPRING
Sugar is an important energy source for proper organism homeostasis and is a highly palatable dietary factor. Clinical and preclinical studies have indicated that excess maternal sugar consumption predisposes to offspring metabolic distribution, but little data point to mental disorders development....
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Published in | Acta neurobiologiae experimentalis Vol. 82; p. LXVIII |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Warsaw
Polish Academy of Sciences
01.01.2022
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Subjects | |
Online Access | Get full text |
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Summary: | Sugar is an important energy source for proper organism homeostasis and is a highly palatable dietary factor. Clinical and preclinical studies have indicated that excess maternal sugar consumption predisposes to offspring metabolic distribution, but little data point to mental disorders development. The aim of our studies were to examine the impact of maternal high-monosaccharide diets (HMDs), during pregnancy and lactation periods, on the offspring's behavioral responses and melanocortin type 4 receptors (MC-4R) expression. Adolescent and young-adult offspring Wistar rats of both sexes after maternal, rich in glucose or fructose, diets were tested in locomotor activity, the novel object recognition, the elevated zero maze, and the forced swimming tests. The MC‑4R gene expression and protein level were measured, using RT-qPCR and ELISA, in several offspring's reward system brain structures at postnatal days 28 and 63. The behavioral observations showed that maternal fructose diet prone to anxiety-like behavior, and increased preferences for curiosity in males. Moreover, HMDs affected at the level of MC-4Rs mRNA and protein depending on the offspring's sexes and ages. Our results showed that perinatal offspring exposure to the maternal HMDs can be a predictor of the development of nervous or/and mental disorders and changes in melanocortin system regulation. |
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ISSN: | 0065-1400 1689-0035 |