Maternal Programming with a Cafeteria Diet Leads to Glucose Intolerance, Increased Insulinemia, Inflammation, and Intestinal Dysbiosis in Rat Offspring

母体通过高蛋白、高糖饮食对后代大鼠进行编程,导致其后代出现葡萄糖耐受不良、胰岛素血症升高、炎症和肠道菌群失调。

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Abstract

The intake of diets high in fat and sugar but low in protein, fiber, and vitamins during pregnancy can contribute to metabolic imbalance, immunological disorders, and intestinal barrier disruption in the offspring. This study investigated the effects of a cafeteria (CAF) diet, high in fat and sugar, consumed throughout pregnancy and lactation, on metabolism, inflammation-related markers, and intestinal microbiota in rat offspring. Maternal programming was conducted for more than 9 weeks in 16 female Wistar rats aged 8-10 weeks. They were divided into two diet groups: control and CAF, each with n=8. On the 21st day after birth, the offspring were weaned, and fecal samples were collected. We conducted a series of glucose and insulin tolerance tests and analyzed serum metabolic markers [triglycerides (TGs), total cholesterol (TC), aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and gamma-glutamyl transferase (GGT)], inflammatory cytokines [monocyte chemoattractant protein-1 (MCP-1/CCL2) and interleukin 6 (IL-6)], and hormones (insulin, leptin, and active ghrelin). Gut microbial profiling was performed to assess compositional changes. The CAF offspring exhibited higher levels of serum glucose, insulin, TGs, MCP-1, and IL-6 compared with the control group. Moreover, the CAF diet altered the intestinal bacterial community structure, increasing the abundance of Prevotellaceae and Lachnospiraceae while reducing Lactobacillaceae. Our results suggest that ingesting a CAF diet during maternal programming promotes adverse impacts on the offspring metabolism homeostasis, inflammatory responses, and intestinal microbiota composition.

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