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Impact of maternal diabetes and snack consumption on offspring food preference

Grant number: 20/03604-8
Support type:Scholarships in Brazil - Scientific Initiation
Effective date (Start): September 01, 2020
Effective date (End): August 31, 2021
Field of knowledge:Health Sciences - Nutrition
Principal Investigator:Ana Carolina Inhasz Kiss
Grantee:Gustavo Venâncio da Silva
Home Institution: Instituto de Biociências (IBB). Universidade Estadual Paulista (UNESP). Campus de Botucatu. Botucatu , SP, Brazil

Abstract

Changes on maternal metabolism and nutrition can increase offspring susceptibility to develop obesity and diabetes. This risk to develop metabolic disorders is also related to offspring nutrition later in life. When animals are given access to different kinds of food, feeding behavior is influenced by food choice/preference. Studies show maternal nutrition can influence offspring food choice. However, the effects of maternal diabetes associated with diet manipulation during pregnancy and lactation on offspring food preference have not been explored. Our hypothesis is that snack consumption will aggravate maternal diabetes, which will compromise offspring brain circuities involved with food preference in a greater degree than seen previously for models of maternal high-fat diet alone. Also, the study will evaluate food preference on both males and females in different life stages (infancy and adulthood) and with 3 different kinds of diet: high-carb, high-protein, and high-fat diets, while most studies currently available explore high-fat and hypercaloric diets only. Preliminary data showed that the experimental model of STZ administration was effective to induce glucose intolerance during pregnancy and that snack consumption exacerbated this effect. Previous studies also show the same treatment has different responses on males and females and the anorectic effects of central insulin infusion are more prominent on offspring of diabetic rats, showing maternal hyperglycemia can impair offspring development of central pathways responsible for control of food intake, reinforcing our hypothesis that food choice will also be compromised.