Abstract
Diabetes mellitus (DM) is a worldwide health concern, and projections state that cases will reach 578 million by 2030. Adjuvant therapies that can help the standard treatment and mitigate DM effects are necessary, especially those using nutritional supplements to improve glycemic control. Previous studies suggest creatine supplementation as a possible adjuvant therapy for DM, but they lack the evaluation of potential morphological parameters alterations and tissue injury caused by this compound. The present study aimed to elucidate clinical, histomorphometric, and histopathological consequences and the cellular oxidative alterations of creatine supplementation in streptozotocin (STZ)-induced type 1 DM rats. We could estimate whether the findings are due to DM or the supplementation from a factorial experimental design. Although creatine supplementation attenuated some biochemical parameters, the morphological analyses of pancreatic and renal tissues made clear that the supplementation did not improve the STZ-induced DM1 injuries. Moreover, creatine-supplemented non-diabetic animals were diagnosed with pancreatitis and showed renal tubular necrosis. Therefore, even in the absence of clinical symptoms and unaltered biochemical parameters, creatine supplementation as adjuvant therapy for DM should be carefully evaluated.
Highlights
We randomly allocated to four groups, with a factorial experimental design (2 × 2): (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
The concentrations in creatinesupplemented non-diabetic animals (CCr) group consumed an average of 3.38 ± 0.13 and 0.56 ± 0.04 g of creatine/animal/day, respectively, in the saturation and maintenance phases
There was no significant difference between the CCr and DCr groups in creatine consumption in both phases
Summary
A hyperglycemic state characterizes DM, usually due to a reduction in circulating insulin levels or a deficit in the tissue effects of this hormone, or both [1,2] This reduction occurs when the pancreas does not produce insulin or when the body cannot use it efficiently [3,4]. T1DM accounts for 5–10% of cases, and Brazil ranks third in the world for new and existing patients of this type [2]. It is characterized by impaired insulin production due to the partial or total destruction of the beta (β) cells, resulting in a progressive deficit of insulin production
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