Consensus document: management of heart failure in type 2 diabetes mellitus.
Heart Fail Rev. 2020 May 24;:
Authors: Kaul U, Ray S, Prabhakar D, Kochar A, Sharma K, Hazra PK, Chandra S, Solanki DRB, Dutta AL, Kumar V, Rao MS, Oomman A, Dani S, Pinto B, Raghu TR
Type 2 diabetes mellitus (T2DM) is a known predisposing factor for heart failure (HF). The growing burden of these two conditions and their impact on health of the individual and on society in general needs urgent attention from the health care professionals. Availability of multiple treatment choices for managing T2DM and HF may make therapeutic decisions more complex for clinicians. Recent cardiovascular outcome trials of antidiabetic drugs have added very robust evidence to effectively manage subjects with this dual condition. This consensus statement provides the prevalence trends and the impact of this dual burden on patients. In addition, it concisely narrates the types of HF, the different treatment algorithms, and recommendations for physicians to comprehensively manage such patients.
PMID: 32447488 [PubMed - as supplied by publisher]
From the gut to the heart: L. plantarum and inulin administration as a novel approach to control cardiac apoptosis via 5-HT2B and TrkB receptors in diabetes.
Clin Nutr. 2020 May 11;:
Authors: Sefidgari-Abrasi S, Roshangar L, Karimi P, Morshedi M, Rahimiyan-Heravan M, Saghafi-Asl M
BACKGROUND & AIMS: Type 2 diabetes mellitus, as a metabolic disorder, can lead to diabetic cardiomyopathy, identified by cardiomyocyte apoptosis and myocardial fibrosis. Brain-derived neurotrophic factor (BDNF) and serotonin are two neurotransmitters that can control cardiomyocyte apoptosis and myocardial fibrosis through their cardiac receptors. In the present study, we investigated the impacts of L. plantarum and inulin supplementation on the inhibition of cardiac apoptosis and fibrosis by modulating intestinal, serum, and cardiac levels of serotonin and BDNF as well as their cardiac receptors.
METHODS: Diabetes was induced by a high-fat diet and streptozotocin in male Wistar rats. Rats were divided into six groups and were supplemented with L. plantarum, inulin or their combination for 8 weeks. Finally, the rats were killed and levels of intestinal, serum, and cardiac parameters were evaluated.
RESULTS: Concurrent administration of L. plantarum and inulin caused a significant rise in the expression of cardiac serotonin and BDNF receptors (P < 0.001) as well as a significant fall in cardiac interstitial and perivascular fibrosis (P < 0.001, both) and apoptosis (P = 0.01). Moreover, there was a strong correlation of cardiac 5-Hydroxytryptamine 2B (5-HT2B) and tropomyosin receptor kinase B (TrkB) receptors with interstitial/perivascular fibrosis and apoptosis (P < 0.001, both).
CONCLUSIONS/INTERPRETATION: Results revealed beneficial effects of L. plantarum, inulin or their combination on intestinal, serum, and cardiac serotonin and BDNF accompanied by higher expression of their cardiac receptors and lower levels of cardiac apoptotic and fibrotic markers. It seems that L. plantarum and inulin supplementation could be considered as a novel adjunct therapy to reduce cardiac complications of type 2 diabetes mellitus.
PMID: 32446786 [PubMed - as supplied by publisher]
Impact of antidiabetic agents on dementia risk: A Bayesian network meta-analysis.
Metabolism. 2020 May 21;:154265
Authors: Zhou JB, Tang X, Dorans KS, Han M, Yang J, Simó R
BACKGROUND: Dementia is more prevalent among people with type 2 diabetes, but little is known regarding the influence of antidiabetic agents on this association.
OBJECTIVE: This study assessed the impact of various antidiabetic agents on the risk of dementia among patients with Type 2 diabetes mellitus.
METHODS: Relevant studies were retrieved from the PubMed, Embase, Cochrane Central Register of Controlled Trials (CENTRAL), and ClinicalTrials.gov databases. Nine antidiabetic agents were included in the search. Data were pooled via network meta-analysis and meta-analysis.
RESULTS: Nine studies were selected for the network meta-analysis with 530,355 individuals and 17 studies for the meta-analysis with 1,258,879 individuals. The analysis excluded glucagon-like peptide 1 (GLP-1) analogs and sodium-dependent glucose transporter 2 (SGLT-2) inhibitors due to the absence of relevant data. The use of dipeptidyl peptidase-4 (DPP-4) inhibitors, metformin, thiazolidinedione, and sulfonylurea was associated with a decreased risk of dementia in comparison to no treatment with antidiabetic agents (hazard ratio [HR] for DPP-4 inhibitors, 0.54; 95% confidence interval [CI], 0.38-0.74, HR for metformin, 0.75; 95% CI, 0.63-0.86; HR for sulfonylurea, 0.85; 95%CI, 0.73-0.98 and HR for thiazolidinedione, 0.70; 95% CI, 0.55-0.89, respectively). However, the node-splitting analysis showed the inconsistency of direct and indirect estimates in sulfonylurea (P=0.042). DPP-4 inhibitors, metformin, thiazolidinedione, and sulfonylurea exhibited a significant impact on the risk of dementia in diabetics compared with insulin (HR, 0.35; 95%CI, 0.20-0.59, HR, 0.48; 95% CI, 0.30-0.77, HR, 0.45; 95% CI, 0.29-0.73 and HR, 0.55; 95% CI, 0.34-0.88, respectively). DPP-4 inhibitors also exhibited a protective effect on the risk of Alzheimer's dementia compared with the no treatment with antidiabetic agents (HR, 0.48; 95% CI, 0.25-0.92). The meta-analysis demonstrated a protective effect of using metformin and DPP-4 inhibitors on the risk of dementia (HR, 0.86; 95% CI, 0.74-1.00 and HR, 0.65; 95% CI, 0.55-0.76, respectively). Further analysis showed insulin was associated with an increased risk of Alzheimer's dementia (HR, 1.60; 95% CI, 1.13-2.26). Only two case-control studies mentioned GLP-1 analogs and SGLT-2 inhibitors, and the pooled ORs showed no evidence of an association with dementia (GLP-1 analogs: 0.71; 95% CI, 0.46-1.10 and SGLT-2 inhibitors: 0.74; 95% CI, 0.47-1.15).
CONCLUSION: This analysis indicated that patients with type 2 diabetes under treatment with DPP-4 inhibitors presented with the lowest risk of dementia, followed by those treated with metformin and thiazolidinedione, while treatment with insulin was associated with the highest risk. For the increasing focus on the protective effect on dementia, further specific clinical studies are needed to evaluate the impact of GLP-1 analogs and SGLT-2 inhibitors on the risk of dementia.
PMID: 32446679 [PubMed - as supplied by publisher]
Fenofibrate decreased microalbuminuria in the type 2 diabetes patients with hypertriglyceridemia.
Lipids Health Dis. 2020 May 23;19(1):103
Authors: Sun X, Liu J, Wang G
BACKGROUND: This study was to research the efficacy of fenofibrate in the treatment of microalbuminuria in the patients with type 2 diabetes mellitus (T2DM) and hypertriglyceridemia.
METHODS: Type 2 diabetic patients (56) with microalbuminuria and hypertriglyceridemia aged 30 to 75 were randomly divided into the fenofibrate treatment group(n = 28) and the control group (n = 28) for 180 days. Urinary microalbumin /creatinine ratio (UACR) and other metabolic parameters were compared at baseline, during treatment and after treatment.
RESULTS: After 180 days, the reduction of level of fasting blood glucose (FBG) and glycosylated hemoglobin (HbA1c) between two groups showed no difference. In the treatment group, uric acid (UA) (296.42 ± 56.41 vs 372.46 ± 72.78), triglyceride (TG) [1.51(1.17, 2.06) vs 3.04(2.21, 3.29)], and UACR [36.45 (15.78,102.41) vs 129.00 (53.00, 226.25)] were significantly decreased compared with the baseline. The high-density lipoprotein cholesterol (HDL-C) levels were significantly increased (1.22 ± 0.26 vs 1.09 ± 0.24) compared with the baseline. The decrease in UACR [- 44.05(- 179.47, - 12.16) vs - 8.15(- 59.69, 41.94)]in treatment group was significantly higher compared with the control group. The decrease in UACR was positively associated with the decreases in TG (r = 0.447, P = 0.042) and UA (r = 0.478, P = 0.024) after fenofibrate treatment.
CONCLUSION: In the patients with hypertriglyceridemia and type 2 diabetes mellitus, fenofibrate can improve microalbuminuria and do not increase the deterioration of glomerular filtration rate.
TRIAL REGISTRATION: ClinicalTrials.gov identifier: NCT02314533, 2014.12.9.
PMID: 32446306 [PubMed - as supplied by publisher]