Banca de DEFESA: MELINE GOMES GONÇALVES

Uma banca de DEFESA de MESTRADO foi cadastrada pelo programa.
STUDENT : MELINE GOMES GONÇALVES
DATE: 25/10/2021
TIME: 14:00
LOCAL: Videoconferência
TITLE:

EVALUATION OF THE EFFECT OF CREATINE SUPPLEMENTATION: A PRECLINICAL STUDY WITH A MODEL OF STREPTOZOTOCIN-INDUCED TYPE I DIABETES

KEY WORDS:

Diabetes mellitus, creatine, kidney, pâncreas, histopathology

PAGES: 78
BIG AREA: Ciências Biológicas
AREA: Bioquímica
SUMMARY:

Diabetes Mellitus (DM) is a chronic metabolic disease growing worldwide. Researches are constantly conducted in an attempt to alleviate the complications of DM and increase the quality of life of patients. Creatine is a nutritional supplement that has been studied for this purpose due to its antioxidant and hypoglycemic features. However, there are no studies reporting the effect of creatine on both metabolism and tissues that may be affected in type I DM. Thus, this study aimed to evaluate the effects of creatine supplementation on symptoms, biochemical and histopathological parameters of the pancreas and kidneys in diabetic rats induced by streptozotocin (STZ). 32 Wistar rats were randomly divided into 4 groups, containing 8 animals each (n=8): (C) normoglycemic animals without creatine supplementation, (CCr) normoglycemic animals with creatine supplementation, (D) diabetic animals induced with STZ without creatine supplementation, (DCr) diabetic animals induced with STZ and supplemented with creatine. Groups D and DCr received a single dose of STZ (40 mg/kg i.p.) for diabetes induction. The CCr and DCr groups received creatine supplementation through isocaloric ration in two phases (saturation, five days before DMI induction, and maintenance, during the 35 days of the experiment, with 13% and 2% creatine, respectively). In order to assess the symptomatology of the pathological condition for all experimental groups, daily water and feed consumption as well as weekly body weight were measured. After anesthesia and euthanasia of the animals, blood and organs were collected and stored for analysis of biochemical parameters [fasting glucose, creatinine, serum urea, aspartate transaminase (AST) and aspartate aminotransferase (ALT)] and histopathological parameters of pancreatic tissues and renal in the animals. In addition to hyperglycemia throughout the experiment, polydipsia, polyphagia and decreased body weight were observed in STZ-induced diabetic animals. Creatine supplementation was able to reduce in animals with DMI and glycemia (p<0,05), the same serum urea and ALT in the DCr group compared to the D group (p<0,01). Histopathologically the pancreatic tissue, where it was observed that the animals in the DCr group did not differ statistically from the animals in the C and CCr groups (p>0,05). In this same group (DCr), the animals dissipated from the islet area compared to group D (p<0,01). For renal tissue the animals in the DCr group reduced reduction in renal glomerulus count compared to the other experimental groups (p<0,05). As for the glomerular areas, the animals in the DCr group were similar to the C and CCr groups, while the animals in the D group had smaller areas of the renal glomeruli (p<0,05). Creatine supplementation in STZ-induced diabetic rats, which induces the DMI experimental model, despite having attenuated the biochemical parameters of glycemia, urea and AST, as well as showing a maintenance and protection of pancreatic histomorphometry, was not able to cause beneficial effects to the DCr group regarding the tissue consequences of DM. On the contrary, CCr has histopathological characteristics referring to tissue damage from both pancreatitis and renal tubular necrosis. Therefore, a creatine supplementation is not feasible in this unpublished experimental archetype. It is evident that more investigations are needed for evidence to add as to its morphological and metabolic effects.

BANKING MEMBERS:
Externo ao Programa - 1667882 - BENTO JOAO DA GRACA AZEVEDO ABREU
Externo à Instituição - DIEGO NEVES ARAUJO - UEPB
Externo ao Programa - 1513597 - JOAO PAULO MATOS SANTOS LIMA