4.Diabetes mellitus and adverse outcomes after carotid endarterectomy: A systematic review and meta-analysis.
Fengshi LI ; Rui ZHANG ; Xiao DI ; Shuai NIU ; Zhihua RONG ; Changwei LIU ; Leng NI
Chinese Medical Journal 2023;136(12):1401-1409
		                        		
		                        			BACKGROUND:
		                        			There is still uncertainty regarding whether diabetes mellitus (DM) can adversely affect patients undergoing carotid endarterectomy (CEA) for carotid stenosis. The aim of the study was to assess the adverse impact of DM on patients with carotid stenosis treated by CEA.
		                        		
		                        			METHODS:
		                        			Eligible studies published between 1 January 2000 and 30 March 2023 were selected from the PubMed, EMBASE, Web of Science, CENTRAL, and ClinicalTrials databases. The short-term and long-term outcomes of major adverse events (MAEs), death, stroke, the composite outcomes of death/stroke, and myocardial infarction (MI) were collected to calculate the pooled effect sizes (ESs), 95% confidence intervals (CIs), and prevalence of adverse outcomes. Subgroup analysis by asymptomatic/symptomatic carotid stenosis and insulin/noninsulin-dependent DM was performed.
		                        		
		                        			RESULTS:
		                        			A total of 19 studies (n = 122,003) were included. Regarding the short-term outcomes, DM was associated with increased risks of MAEs (ES = 1.52, 95% CI: [1.15-2.01], prevalence = 5.1%), death/stroke (ES = 1.61, 95% CI: [1.13-2.28], prevalence = 2.3%), stroke (ES = 1.55, 95% CI: [1.16-1.55], prevalence = 3.5%), death (ES = 1.70, 95% CI: [1.25-2.31], prevalence =1.2%), and MI (ES = 1.52, 95% CI: [1.15-2.01], prevalence = 1.4%). DM was associated with increased risks of long-term MAEs (ES = 1.24, 95% CI: [1.04-1.49], prevalence = 12.2%). In the subgroup analysis, DM was associated with an increased risk of short-term MAEs, death/stroke, stroke, and MI in asymptomatic patients undergoing CEA and with only short-term MAEs in the symptomatic patients. Both insulin- and noninsulin-dependent DM patients had an increased risk of short-term and long-term MAEs, and insulin-dependent DM was also associated with the short-term risk of death/stroke, death, and MI.
		                        		
		                        			CONCLUSIONS
		                        			In patients with carotid stenosis treated by CEA, DM is associated with short-term and long-term MAEs. DM may have a greater impact on adverse outcomes in asymptomatic patients after CEA. Insulin-dependent DM may have a more significant impact on post-CEA adverse outcomes than noninsulin-dependent DM. Whether DM management could reduce the risk of adverse outcomes after CEA requires further investigation.
		                        		
		                        		
		                        		
		                        			Humans
		                        			;
		                        		
		                        			Endarterectomy, Carotid/adverse effects*
		                        			;
		                        		
		                        			Carotid Stenosis/surgery*
		                        			;
		                        		
		                        			Risk Factors
		                        			;
		                        		
		                        			Treatment Outcome
		                        			;
		                        		
		                        			Time Factors
		                        			;
		                        		
		                        			Stents/adverse effects*
		                        			;
		                        		
		                        			Diabetes Mellitus, Type 2/complications*
		                        			;
		                        		
		                        			Diabetes Mellitus, Type 1
		                        			;
		                        		
		                        			Stroke/complications*
		                        			;
		                        		
		                        			Insulin/therapeutic use*
		                        			;
		                        		
		                        			Myocardial Infarction/complications*
		                        			;
		                        		
		                        			Risk Assessment
		                        			
		                        		
		                        	
6.Continuous Blood Glucose Monitoring:Technological Progress and Application Extension.
Chinese Journal of Medical Instrumentation 2023;47(4):424-427
		                        		
		                        			
		                        			Continuous glucose monitoring (CGM) technology developed rapidly in recent years, and new products came out all the time. Nowadays, CGM plays an important role in diabetes management and has been recommended by various guideline all over the world. CGM equipment classification, progress on glucose sensor technology, and the new application and expansion of CGM technology in the field of diabetes and non-diabetes were briefly introduced in the study.
		                        		
		                        		
		                        		
		                        			Humans
		                        			;
		                        		
		                        			Diabetes Mellitus, Type 1
		                        			;
		                        		
		                        			Blood Glucose
		                        			;
		                        		
		                        			Blood Glucose Self-Monitoring
		                        			;
		                        		
		                        			Technology
		                        			
		                        		
		                        	
8.Dihydromyricetin improves Parkinson's disease-like lesions in T2DM rats by activating AMPK/ULK1 pathway.
Qi LI ; Nian CHEN ; Jin-Ding LUO ; Hui-Lin WU ; Zi-Han WANG ; Meng-Wei LI ; Shui-Dong FENG ; Hong-Yan LING
Acta Physiologica Sinica 2023;75(1):59-68
		                        		
		                        			
		                        			The purpose of this study was to explore the effect and mechanism of dihydromyricetin (DHM) on Parkinson's disease (PD)-like lesions in type 2 diabetes mellitus (T2DM) rats. The T2DM model was established by feeding Sprague Dawley (SD) rats with high-fat diet and intraperitoneal injection of streptozocin (STZ). The rats were intragastrically administered with DHM (125 or 250 mg/kg per day) for 24 weeks. The motor ability of the rats was measured by balance beam experiment, the changes of dopaminergic (DA) neurons and the expression of autophagy initiation related protein ULK1 in the midbrains of the rats were detected by immunohistochemistry, and the protein expression levels of α-synuclein (α-syn), tyrosine hydroxylase (TH), as well as AMPK activation level, in the midbrains of the rats were detected by Western blot. The results showed that, compared with normal control, the rats with long-term T2DM exhibited motor dysfunction, increased α-syn aggregation, down-regulated TH protein expression, decreased number of DA neurons, declined activation level of AMPK, and significantly down-regulated ULK1 expression in the midbrain. DHM (250 mg/kg per day) treatment for 24 weeks significantly improved the above PD-like lesions, increased AMPK activity, and up-regulated ULK1 protein expression in T2DM rats. These results suggest that DHM may improve PD-like lesions in T2DM rats by activating AMPK/ULK1 pathway.
		                        		
		                        		
		                        		
		                        			Rats
		                        			;
		                        		
		                        			Animals
		                        			;
		                        		
		                        			Parkinson Disease
		                        			;
		                        		
		                        			Rats, Sprague-Dawley
		                        			;
		                        		
		                        			AMP-Activated Protein Kinases
		                        			;
		                        		
		                        			Diabetes Mellitus, Type 2
		                        			;
		                        		
		                        			Autophagy-Related Protein-1 Homolog
		                        			
		                        		
		                        	
9.Zuogui Jiangtang Qinggan Prescription promotes recovery of intestinal mucosal barrier in mice with type 2 diabetes mellitus and nonalcoholic fatty liver disease by improving intestinal flora homeostasis.
Jun-Ju ZOU ; Hong LI ; Min ZHOU ; Qiu-Qing HUANG ; Yong-Jun WU ; Rong YU
China Journal of Chinese Materia Medica 2023;48(2):525-533
		                        		
		                        			
		                        			This study aimed to investigate the recovery effect of Zuogui Jiangtang Qinggan Prescription on intestinal flora homeostasis control and intestinal mucosal barrier in type 2 diabetes mellitus(T2DM) with nonalcoholic fatty liver disease(NAFLD) induced by a high-fat diet. NAFLD was established in MKR transgenic mice(T2DM mice) by a high-fat diet(HFD), and subsequently treated for 8 weeks with Zuogui Jiangtang Qinggan Prescription(7.5, 15 g·kg~(-1)) and metformin(0.067 g·kg~(-1)). Triglyceride and liver function were assessed using serum. The hematoxylin-eosin(HE) staining and Masson staining were used to stain the liver tissue, while HE staining and AB-PAS staining were used to stain the intestine tissue. 16S rRNA sequencing was utilized to track the changes in the intestinal flora of the mice in each group. Polymerase chain reaction(PCR) and immunofluorescence were used to determine the protein and mRNA expression levels of ZO-1, Occludin, and Claudin-1. The results demonstrated that Zuogui Jiangtang Qinggan Prescription increased the body mass of T2DM mice with NAFLD and decreased the hepatic index. It down-regulated the serum biomarkers of liver function and dyslipidemia such as alanine aminotransferase(ALT), aspartate transaminase(AST), and triglycerides(TG), increased insulin sensitivity, and improved glucose tolerance. According to the results of 16S rRNA sequencing, the Zuogui Jiangtang Qinggan Prescription altered the composition and abundance of the intestinal flora, increasing the relative abundances of Muribaculaceae, Lactobacillaceae, Lactobacillus, Akkermansia, and Bacteroidota and decreasing the relative abundances of Lachnospiraceae, Firmicutes, Deslfobacteria, Proteobacteria, and Desulfovibrionaceae. According to the pathological examination of the intestinal mucosa, Zuogui Jiangtang Qinggan Prescritpion increased the expression levels of the tight junction proteins ZO-1, Occludin, and Claudin-1, promoted intestinal mucosa repair, protected intestinal villi, and increased the height of intestinal mucosa villi and the number of goblet cells. By enhancing intestinal mucosal barrier repair and controlling intestinal microbiota homeostasis, Zuogui Jiangtang Qinggan Prescription reduces intestinal mucosal damage induced by T2DM and NAFLD.
		                        		
		                        		
		                        		
		                        			Mice
		                        			;
		                        		
		                        			Animals
		                        			;
		                        		
		                        			Non-alcoholic Fatty Liver Disease/metabolism*
		                        			;
		                        		
		                        			Gastrointestinal Microbiome
		                        			;
		                        		
		                        			RNA, Ribosomal, 16S
		                        			;
		                        		
		                        			Diabetes Mellitus, Type 2/metabolism*
		                        			;
		                        		
		                        			Occludin/pharmacology*
		                        			;
		                        		
		                        			Claudin-1/metabolism*
		                        			;
		                        		
		                        			Intestinal Mucosa
		                        			;
		                        		
		                        			Liver
		                        			;
		                        		
		                        			Triglycerides/metabolism*
		                        			;
		                        		
		                        			Diet, High-Fat
		                        			;
		                        		
		                        			Homeostasis
		                        			;
		                        		
		                        			Mice, Inbred C57BL
		                        			
		                        		
		                        	
10.Mulberry leaf flavonoids activate BAT and induce browning of WAT to improve type 2 diabetes via regulating the AMPK/SIRT1/PGC-1α signaling pathway.
Long CHENG ; Lu SHI ; Changhao HE ; Chen WANG ; Yinglan LV ; Huimin LI ; Yongcheng AN ; Yuhui DUAN ; Hongyu DAI ; Huilin ZHANG ; Yan HUANG ; Wanxin FU ; Weiguang SUN ; Baosheng ZHAO
Chinese Journal of Natural Medicines (English Ed.) 2023;21(11):812-829
		                        		
		                        			
		                        			Mulberry (Morus alba L.) leaf is a well-established traditional Chinese botanical and culinary resource. It has found widespread application in the management of diabetes. The bioactive constituents of mulberry leaf, specifically mulberry leaf flavonoids (MLFs), exhibit pronounced potential in the amelioration of type 2 diabetes (T2D). This potential is attributed to their ability to safeguard pancreatic β cells, enhance insulin resistance, and inhibit α-glucosidase activity. Our antecedent research findings underscore the substantial therapeutic efficacy of MLFs in treating T2D. However, the precise mechanistic underpinnings of MLF's anti-T2D effects remain the subject of inquiry. Activation of brown/beige adipocytes is a novel and promising strategy for T2D treatment. In the present study, our primary objective was to elucidate the impact of MLFs on adipose tissue browning in db/db mice and 3T3-L1 cells and elucidate its underlying mechanism. The results manifested that MLFs reduced body weight and food intake, alleviated hepatic steatosis, improved insulin sensitivity, and increased lipolysis and thermogenesis in db/db mice. Moreover, MLFs activated brown adipose tissue (BAT) and induced the browning of inguinal white adipose tissue (IWAT) and 3T3-L1 adipocytes by increasing the expressions of brown adipocyte marker genes and proteins such as uncoupling protein 1 (UCP1) and beige adipocyte marker genes such as transmembrane protein 26 (Tmem26), thereby promoting mitochondrial biogenesis. Mechanistically, MLFs facilitated the activation of BAT and the induction of WAT browning to ameliorate T2D primarily through the activation of AMP-activated protein kinase (AMPK)/sirtuin 1 (SIRT1)/peroxisome proliferator-activated receptor-gamma coactivator 1α (PGC-1α) signaling pathway. These findings highlight the unique capacity of MLF to counteract T2D by enhancing BAT activation and inducing browning of IWAT, thereby ameliorating glucose and lipid metabolism disorders. As such, MLFs emerge as a prospective and innovative browning agent for the treatment of T2D.
		                        		
		                        		
		                        		
		                        			Mice
		                        			;
		                        		
		                        			Animals
		                        			;
		                        		
		                        			Adipose Tissue, Brown
		                        			;
		                        		
		                        			Sirtuin 1/pharmacology*
		                        			;
		                        		
		                        			Diabetes Mellitus, Type 2/metabolism*
		                        			;
		                        		
		                        			AMP-Activated Protein Kinases/metabolism*
		                        			;
		                        		
		                        			Morus/metabolism*
		                        			;
		                        		
		                        			Flavonoids/metabolism*
		                        			;
		                        		
		                        			Prospective Studies
		                        			;
		                        		
		                        			Signal Transduction
		                        			;
		                        		
		                        			Adipose Tissue, White
		                        			;
		                        		
		                        			Plant Leaves
		                        			;
		                        		
		                        			Uncoupling Protein 1/metabolism*
		                        			;
		                        		
		                        			Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism*
		                        			
		                        		
		                        	
            
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