China
Africa
Explore chapters and articles related to this topic
The Management of Patients with Heart Failure and Diabetes
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
The EMPA-REG OUTCOME trial was the first study to provide evidence of improved HF outcomes with a drug (empagliflozin), the target population of which was diabetics. Empagliflozin belongs to the SGLT-2 inhibitor family. In the kidneys, SGLT-2 serves as a sodium-glucose cotransporter and reabsorbs about 90% of the glucose, while promoting natriuresis. SGLT-2 inhibitors block this channel, enhancing glucosuria. Worsening hyperglycemia augments their function, whereas lower glucose level diminishes their efficacy, decreasing the risk of hypoglycemia with SGLT-2 inhibitors alone. However, the risk of hypoglycemia increases when SGLT-2 inhibitors are combined with insulin or insulin secretagogues, such as sulfonylureas.33
Allopathic Medicines
Published in Varma H. Rambaran, Nalini K. Singh, Alternative Medicines for Diabetes Management, 2023
Varma H. Rambaran, Nalini K. Singh
Symptomatic side effects that include mostly urinary or genital irritation or infections are common but tolerated by most patients. Importantly, the new SGLTi drugs have highly desirable and somewhat unexpected cardiac and renal protective effects, at least in selected cohorts. Large trials of empagliflozin (Figure 2.18a) and canagliflozin (Invokana) (Figure 2.18b), aiming to demonstrate safety in patients with T2DM and high cardiovascular risk, have shown favourable effects on heart failure, cardiovascular death, and the progression of albuminuria. Unwanted side effects, such as dehydration, lower extremity amputations, and diabetic ketoacidosis (DKA), have also been reported, but have been noted as very rare (Riddle and Cefalu 2018).Structural formulae of SGLTi drugs: (a) empagliflozin, (b) canagliflozin, (c) dapagliflozin, and (d) ertugliflozin.
Heart failure
Published in Henry J. Woodford, Essential Geriatrics, 2022
Empagliflozin has also been tested against placebo in people with HFpEF (n = 5,988; mean age 72; 49% had diabetes; median follow-up 26 months).46 People recruited had an EF > 40% (mean 54%; 33% of people in range 40–50%). The primary composite outcome of cardiovascular death or hospitalisation for heart failure favoured empagliflozin (HR 0.79; 95% CI 0.69–0.90; 13.8% v 17.1%; NNT = 66 per year), mainly through reduced hospitalisations. The effect size was largest for people with EF < 50%. However, death or hospitalisation for any cause were not significantly reduced, suggesting no net prognostic benefit. Adverse events reported more frequently with empagliflozin included hypotension (10.4% v 8.6%), urinary tract infections (9.9% v 8.1%) and genital infections (2.2% v 0.7%).
Sodium-glucose transporter (SGLT2) inhibition: A potential target for treatment of type-2 Diabetes Mellitus with Natural and Synthetic compounds
Published in Egyptian Journal of Basic and Applied Sciences, 2023
Shubham Batra, Prabhjeet Kaur Bamrah, Manjusha Choudhary
For the treatment of individuals with type 2 diabetes mellitus, Empagliflozin, a subclass of Gliflozin (FDA approved in 2014), is extremely successful and well-tolerated in many nations, including the EU, the USA, Japan, and others. It exerts higher selectivity for SGLT2 (>2500-fold) over SGLT1 compared to other SGLT2 inhibitors [23,24]. The medication lowers the kidneys’ glucose threshold and limits the reabsorption of filtered glucose because it inhibits SGLT2, which raises urinary glucose excretion and decreases blood glucose levels, and also suppressed SGLT2 in a dose-dependent manner. Moreover, in the clinical trials, participants tolerated empagliflozin well, with most adverse events being mild or moderate in severity. Empagliflozin is mostly metabolized in humans by glucuronidation by 50-uridine diphosphoglucuronosyltransferases (UGTs) 1A3, 1A8, 1A9, and 2B7 and about 54% was eliminated as an unaltered drug in the urine [25].
The antioxidative effects of empagliflozin on high glucose‑induced epithelial-mesenchymal transition in peritoneal mesothelial cells via the Nrf2/HO-1 signaling
Published in Renal Failure, 2022
Ping Shi, Zhoubing Zhan, Xiaojie Ye, Ying Lu, Kai Song, Feng Sheng, Huaying Shen, Peiran Yin
To evaluate the effects of empagliflozin in vivo, a rat model of peritoneal fibrosis was established by daily intraperitoneal injection of the 4.25% glucose PDS. Compared with the control and Emp groups, the PD group exhibited significant characteristics of peritoneal fibrosis. The current study demonstrated that empagliflozin could notably improve peritoneal function, relieve the thickness of the peritoneum and ameliorate collagen accumulation. Moreover, empagliflozin was able to inhibit the EMT by promoting the expression of epithelial marker E-cadherin and inhibiting the expression of fibrotic markers, including α-SMA, Collagen-I, and Fibronectin. Our previous study investigated the effects of varying empagliflozin concentrations (1, 3, and 6 mg/kg) on peritoneal glucose uptake in rats and found that rats with empagliflozin concentrations of 3 mg/kg reached the highest levels of both peritoneal glucose uptake ratios at D4/D0 and ultrafiltration ratios. Accordingly, the dose of empagliflozin used was 3 mg/kg in our study[18].
Empagliflozin alleviates myocardial I/R injury and cardiomyocyte apoptosis via inhibiting ER stress-induced autophagy and the PERK/ATF4/Beclin1 pathway
Published in Journal of Drug Targeting, 2022
Cuan-Cuan Wang, Ying Li, Xiao-Qian Qian, Hui Zhao, Dong Wang, Guo-Xing Zuo, Kuan Wang
Empagliflozin is an inhibitor of SGLT2 and has been approved to be used as a medication for type 2 diabetes to reduce the level of blood sugar [33]. Besides glycaemic control, growing evidence has shown that empagliflozin helps reduce cardiovascular mortality in patients with diabetes [34]. Intriguingly, empagliflozin lowers the risk of death of heart failure in non-diabetic patients [35]. Recently, Lu et al. reported that empagliflozin ameliorated myocardial I/R injury by regulating the LKB1/AMPK signalling [14]. In addition, empagliflozin alleviated cerebral I/R injury-induced neuronal apoptosis [36]. However, the effect of empagliflozin on myocardial I/R injury-induced cardiomyocyte apoptosis has not been reported yet. In this study, we demonstrated that empagliflozin alleviated myocardial I/R injury-induced cardiomyocyte apoptosis in vivo and H2O2-induced cardiomyocyte apoptosis in vitro for the first time, providing novel evidence that empagliflozin contributes to suppressing myocardial I/R injury. Combining with previous clinical and preclinical studies, our findings show that empagliflozin has great clinical significance in alleviating myocardial I/R injury through suppression of cardiomyocyte apoptosis in both diabetic and nondiabetic conditions.