| Grant number: | 22/11249-9 |
| Support Opportunities: | Scholarships in Brazil - Doctorate (Direct) |
| Start date: | December 01, 2022 |
| End date: | August 31, 2026 |
| Field of knowledge: | Biological Sciences - Physiology - Physiology of Organs and Systems |
| Principal Investigator: | Rui Curi |
| Grantee: | Gabriela Mandu Gimenes |
| Host Institution: | Centro de Ciências Biológicas e da Saúde. Universidade Cruzeiro do Sul (UNICSUL). São Paulo , SP, Brazil |
| Associated research grant: | 18/09868-7 - CELLULAR AND MOLECULAR MECHANISMS OF INSULIN RESISTANCE AND INFLAMMATION IN OBESE WISTAR RATS AND LEAN GOTO-KAKIZAKI RATS: Causes and associations with diet and physcial exercise, AP.TEM |
| Associated scholarship(s): | 23/14878-0 - ASSOCIATION OF GUT MICROBIOTA WITH THE DIABETIC PHENOTYPE OF GOTO-KAKIZAKI RAT (A NON-OBESE DIABETIC MODEL), BE.EP.DD |
Abstract The Goto-Kakizaki (GK) rat spontaneously develops Type 2 Diabetes Mellitus (T2DM) but without obesity. In GK rats, we reported slow intestinal transit and increased small intestinal pro-inflammatory markers. The myenteric plexus is part of the enteric nervous system (ENS) and controls intestinal motility. The myenteric of small intestine pf GK rats has differences regarding the density of inhibitory neurons in the duodenum (decreased) and jejunum (increased). The diabetic state, in turn, causes marked changes in SNE and the intestinal microbiota. We believe that the slower intestinal transit (constipation) can trigger insulin resistance (IR) and T2DM in GK rats by promoting changes in the microbiota composition. We will investigate this hypothesis in the same animal at different ages (weaning- 21, 60, and 120 days). During the experimental period, we will measure the following parameters: intestinal motility by methylene blue gavage, determination of plasma LPS (lipopolysaccharides), metagenomic analysis of microbiota composition, and peripheral sensitivity to insulin through glucose and insulin tolerance tests. An antibiotic cocktail will be administered to the animals from weaning to 60 days old to induce depletion of the intestinal microbiota in GK and Wistar rats. With this protocol, it will be possible to investigate the influence of the intestinal microbiota on the genesis of the diabetic phenotype of GK rats. After the treatment, peripheral insulin sensitivity and intestinal permeability and motility will be evaluated. The total population of neurons (HuC/D) and the inhibitory (nNOS) and excitatory (ChAT) subpopulations as well as the glia (S100) of the myenteric plexus will be studied by immunofluorescence in a whole mount preparation. | |
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