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Introduction: Type 1 diabetes mellitus (T1DM) is characterized by an absolute deficiency of insulin and dependence on insulin therapy. Therefore, glycemic control and management are important for T1DM patients, particularly glycemic variability, which is associated with the development of diabetic complications. However, insufficient attention has been paid to the glycemic variability in T1DM patients so far. Our objective was to identify the effects of food intake on glycemic variability in T1DM patients. Methods: This was a single-center study that took place in the outpatient clinics of Peking Union Medical College Hospital. A total of 68 Chinese T1DM patients between June 2018 and June 2019 were enrolled. After the baseline demographic and clinical characteristics were evaluated, each participant underwent 14-day flash glucose monitoring (FGM). They recorded caloric intake of breakfast, lunch, and dinner at least 3 days/week using a "Menthol Health" app. After 2 weeks, we obtained the FGM data and did further data analysis. Baseline characteristics and glycemic variability index generated by FGM were compared among groups. A general linear model was used to compare data among groups after adjusting for potential confounding factors. The quantitative relationship between two continuous variables was explored by constructing a linear regression equation. Results: The results showed that the C-peptide level was independently correlated with the mean of daily differences (MODD) after adjusting for the possible confounders (β = − 0.239, p = 0.046). The dietary nutrition intake had no effect on glycemic variability. However, the nutritional composition of carbohydrate, fat, and protein was an independent risk factor for time spent in hypoglycemia (TBR) post adjustment (β = − 0.213, p = 0.054). However, there was no impact of daily total energy intake on glycemic variability index. Conclusion: In our study, dietary nutrition intake had no effect on glycemic variability, but residual β-cell function was identified as an influencing factor for glycemic variability in T1DM adults. However, nutritional macronutrient composition played some roles in the occurrence of hypoglycemia. This might provide new evidence for the clinical glycemic control and management of T1DM in the Chinese population. [ABSTRACT FROM AUTHOR]

Insulin and liraglutide have been demonstrated to control blood glucose and exert neuroprotective effects. However, the impact of liraglutide or insulin alone or in combination on brain pathology in type 1 diabetes mellitus (T1DM) and their underlying mechanisms are unclear. In the present study, diabetes mellitus (DM) was induced via intraperitoneal injection of streptozotocin in mice and subsequently mice were treated with insulin, liraglutide, a combination of the two drugs or saline. Changes in body weight and blood glucose were assessed weekly. The pathological changes in the brain tissue and the apoptosis of neurons were assessed using H&E staining and TUNEL staining. The mRNA and protein expression levels of apoptosis-related proteins were detected using reverse transcription-quantitative PCR (RT-qPCR) and western blotting, respectively. Moreover, Ki67 protein expression was analyzed using immunohistochemistry and the mRNA and protein expression levels of Wnt/β-catenin signaling pathway-related proteins were examined using RT-qPCR and western blotting, respectively. The results of the present study suggested that DM mice developed hyperglycemia and weight loss and also exhibited significantly increased neural cell apoptosis and significantly reduced numbers of Ki67-positive cells. Liraglutide significantly decreased blood glucose levels in DM mice, whereas both insulin and the combination of the two drugs failed to control blood glucose well. Insulin, liraglutide and their combination also failed to control body weight well, but significantly attenuated brain pathological changes and activation of the pro-apoptotic proteins Caspase-3 and Bax, which may have resulted in the significant increase in the expression levels of Wnt/β-catenin signaling pathway-associated molecules such as Wnt3a and S9-pGSK-3β. Liraglutide also promoted the protein expression of the neurogenesis marker of Ki67 and the antiapoptotic factor Bcl-2. These results suggested that insulin and liraglutide may improve brain damage via upregulation of the Wnt/β-catenin signaling pathway and could be of therapeutic relevance for improvement of cognitive impairment in patients with DM. [ABSTRACT FROM AUTHOR]