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Metabolic changes in female rats exposed to intrauterine hyperglycemia and postweaning consumption of high-fat diet
- Source :
- Web of Science, Repositório Institucional da UNESP, Universidade Estadual Paulista (UNESP), instacron:UNESP
- Publication Year :
- 2021
- Publisher :
- Oxford University Press (OUP), 2021.
-
Abstract
- Made available in DSpace on 2022-04-28T17:22:59Z (GMT). No. of bitstreams: 0 Previous issue date: 2021-10-20 Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) We evaluated the influence of the hyperglycemic intrauterine environment and postweaning consumption of a high-fat diet (HFD) on the glycemia, insulin, lipid, and immunological profile of rat offspring in adulthood. Female rats received citrate buffer (Control-C) or Streptozotocin (a beta cell-cytotoxic drug to induce diabetes-D) on postnatal day 5. In adulthood, these rats were mated to obtain female offspring, who were fed a standard diet (SD) or HFD from weaning to adulthood (n = 10 rats/group). OC/SD and OC/HFD represent female offspring of control mothers and received SD or HFD, respectively; OD/SD and OD/HFD represent female offspring of diabetic mothers and received SD or HFD, respectively. At adulthood, the oral glucose tolerance test (OGTT) was performed and, next, the rats were anesthetized and euthanized. Pancreas was collected and analyzed, and adipose tissue was weighted. Blood samples were collected to determine biochemical and immunological profiles. The food intake was lower in HFD-fed rats and visceral fat weight was increased in the OD/HFD group. OC/HFD, OD/SD, and OD/HFD groups presented glucose intolerance and lower insulin secretion during OGTT. An impaired pancreatic beta-cell function was shown in the adult offspring of diabetic rats, regardless of diet. Interleukin (IL)-6 and IL-10 concentrations were lower in the OD/HFD group and associated to a low-grade inflammatory condition. The fetal programming was responsible for impaired beta cell function in experimental animals. The association of maternal diabetes and postweaning HFD are responsible for greater glucose intolerance, impaired insulin secretion and immunological change. Summary sentence Summary Sentence The association of maternal diabetes and postweaning HFD causes glucose intolerance due to beta-cell disarrangement and impaired insulin secretion, and immunological changes in adult offspring. SJo Paulo State Univ UNESP, Botucatu Med Sch, Lab Expt Res Gynecol & Obstet, Tocogynecol Postgrad Course, Botucatu, SP, Brazil Fed Univ Mato Grosso UFMT, Inst Biol & Hlth Sci, Lab Syst Physiol & Reprod Toxicol, Barra Do Garcas, MT, Brazil Fed Univ Maranhao UFMA, Dept Physiol Sci, Lab Expt Physiol, Sao Luis, MA, Brazil Univ Estadual Paulista UNESP, Botucatu Med Sch, Res Support Off, Botucatu, SP, Brazil SJo Paulo State Univ UNESP, Botucatu Med Sch, Lab Expt Res Gynecol & Obstet, Tocogynecol Postgrad Course, Botucatu, SP, Brazil Univ Estadual Paulista UNESP, Botucatu Med Sch, Res Support Off, Botucatu, SP, Brazil FAPESP: 2016/25207-5
- Subjects :
- medicine.medical_specialty
Offspring
medicine.medical_treatment
Pregnancy in Diabetics
Adipose tissue
Weaning
Biology
Diet, High-Fat
Diabetes Mellitus, Experimental
Rats, Sprague-Dawley
Pregnancy
Insulin-Secreting Cells
Diabetes mellitus
Internal medicine
Glucose Intolerance
medicine
Animals
rat
Adiposity
diabetes
Insulin
digestive, oral, and skin physiology
food and beverages
nutritional and metabolic diseases
Interleukin
Cell Biology
General Medicine
medicine.disease
Streptozotocin
Rats
Pregnancy Complications
fetal programming
high-fat diet
Endocrinology
medicine.anatomical_structure
Reproductive Medicine
Hyperglycemia
Prenatal Exposure Delayed Effects
Female
lipids (amino acids, peptides, and proteins)
Insulin Resistance
Pancreas
hormones, hormone substitutes, and hormone antagonists
medicine.drug
Subjects
Details
- ISSN :
- 15297268 and 00063363
- Volume :
- 106
- Database :
- OpenAIRE
- Journal :
- Biology of Reproduction
- Accession number :
- edsair.doi.dedup.....a368f103c193f4595298af32b1d3f7af
- Full Text :
- https://doi.org/10.1093/biolre/ioab195