Effects of diet‐induced obesity on the expression patterns of a lactoferrin receptor variant, omentin‐1, in growing mice (133.2)

Abstract

The pathophysiology ascribed to increased adiposity is due in part to perturbation of tissue‐specific and systemic levels of pleiotropic cytokines. A circulating variant of the lactoferrin receptor (LfR), known as omentin‐1, a novel adipokine, is differentially expressed in humans with metabolic disease (e.g., type II diabetes) and aberrant immune activation (e.g., Crohn’s disease); however, the cellular origin(s) and effector function(s) of omentin‐1 remain to be fully elucidated. We investigated the effect of diet‐induced obesity (DIO) on omentin‐1 expression patterns in growing mice. At 28 days postpartum, male C57BL/6N mice were fed a control (CTRL: 10% fat) or a high fat‐sucrose (HFS: 45% fat) diet for 14 wks. Protein analysis showed that omentin‐1 was constitutively expressed across various tissues. HFS‐fed animals gained more weight (~20%) than CTRL‐fed animals by 14 wk. Using oral glucose‐ and i.p. insulin tolerance tests, these animals were shown to display marked glucose intolerance at 4, 8, and 12 wk and insulin resistance at 5, 9, and 13 wk. HFS‐fed animals had increased plasma leptin at 6, 10, and 14 wk and elevated hepatic triglycerides at 14 wk. Fasting omentin‐1 concentrations were higher in CTRL‐fed animals at 4 wk compared to HFS‐fed animals but not later, suggesting that omentin‐1 expression patterns are modulated by DIO in young mice and may signal an early alteration in global inflammatory status.