Recent good papers:
Empagliflozin rescues lifespan and liver senescence in naturally aged mice 2024
Our study revealed that empagliflozin improved survival and health in naturally aged mice. Empagliflozin extended the median survival of male mice by 5.9%. Meanwhile, empagliflozin improved learning memory and motor balance, decreased body weight, and downregulated the hepatic protein expression of P21, P16, α-SMA, and COL1A1. Empagliflozin modulates the structure of the intestinal flora, increasing the relative abundance of Lachnospiraceae, Ruminococcaceae, Lactobacillus, Blautia, and Muribaculaceae and decreasing the relative abundance of Erysipelotrichaceae, Turicibacter, and Dubosiella in naturally aged mice. Further exploration discovered that empagliflozin increased the concentration of SCFAs, decreased the levels of the inflammatory factors TNF-α, IL-6, and CXCL9, and regulated the PI3K/AKT/P21 and AMPK/SIRT1/NF-κB pathways, which may represent the underlying mechanisms involved in these beneficial hepatic effects. Taken together, the above results indicated that empagliflozin intervention could be considered a potential strategy for extending lifespan and slowing liver senescence in naturally aged mice.
Comparative cardiovascular and renal effectiveness of empagliflozin and dapagliflozin: scandinavian cohort study 2024
Use of empagliflozin and dapagliflozin was associated with similar risk of cardiovascular and renal outcomes, mortality and diabetic ketoacidosis.
Head-to-Head Comparison of Dapagliflozin vs. Empagliflozin—Cardiovascular and Safety Events 2024
Dapagliflozin has similar CV benefits at doses proven effective in cardiovascular outcome trials, i.e., dapagliflozin 10mg, but the 5 mg dose may not have similar CV effectiveness.
SGLT2i effect on atrial fibrillation: A network meta-analysis of randomized controlled trials 2024
Dapagliflozin use was associated with significant reduction in AF risk as compared to placebo in overall population and patients with diabetes, whereas the use of other gliflozins did not significantly reduce AF occurrence.
Dapagliflozin: A sodium–glucose cotransporter 2 inhibitor, attenuates angiotensin II-induced atrial fibrillation by regulating atrial electrical and structural remodeling 2024
Overall, our study identifies DAPA, a widely used SGLT2i, contributes to inhibiting Ang II-induced ox-CaMKII upregulation and electrical and structural remodeling to reduce AF susceptibility, suggesting that DAPA may be a potential therapy of treating AF.
SGLT2 Inhibitor Dapagliflozin Increases Skeletal Muscle and Brain Fatty Acid Uptake in Individuals With Type 2 Diabetes: A Randomized Double-Blind Placebo-Controlled Positron Emission Tomography Study 2024
Six weeks of treatment with dapagliflozin increases skeletal muscle and brain FA uptake, partly driven by a rise in free FA availability. This finding is in accordance with previous indirect measurements showing enhanced FA metabolism in response to SGLT2 inhibition and extends the notion of a shift toward increased FA use to muscle and brain.
Glycemic Variability after Initiation of SGLT2 Inhibitors in CKD 2024
In a pilot study, we enrolled 11 CKD patients with clinical indications for SGLT2i -7 with type 2 diabetes not on insulin, and 4 without diabetes. Participants wore DexCom G6 CGM for 10 days pre-SGLT2i and another 10 days post-SGLT2i initiation. […] Nine participants received empagliflozin 10mg, two dapagliflozin 10mg. Following SGLT2i initiation, participants with diabetes showed no significant change in mean glucose (160±54 vs 155±50 mg/dL, p=0.52), GMI (7.1±1.3 vs 7.0±1.2, p=0.52), or TIR (67±37 vs 69±39%, p=0.66). There was no change in time above range or time below range. Only 1 participant on GLP-1 receptor agonist developed asymptomatic level 1 hypoglycemia. Similarly, patients without diabetes had no change in any of the previously mentioned CGM metrics. However, glycemic variability decreased post-SGLT2i initiation, as shown by hourly CV reductions (-0.40±0.13, p=0.002). The magnitude of hourly CV reduction was more pronounced in participants without diabetes compared to those with diabetes (p-interaction=0.002). Despite higher hourly CV during daytime than nighttime, the impact of SGLT2i initiation on CV was similar across time periods without significant interaction by time of day. […] After SGLT2i initiation in CKD, while mean glycemia and TIR remained unchanged, glycemic variability diminished. This finding warrants further investigation in a larger study.
Effects of Dapagliflozin and Metformin on Vascular Function in Newly Diagnosed Type 2 Diabetes—A Randomized Controlled Trial (DMVascular Study) 2024
Initial treatment with Dapagliflozin gives a better response than Metformin for CIMT. Larger-scale longitudinal studies will clarify the potential of SGLT-2 inhibitors as initial diabetes pharmacotherapy.
(SGLT2 + GLP1RA combination, poke @DrFraser =>)
Changes in Beta-Cell Function during Dapagliflozin Therapy in Combination with Exenatide in Type 2 Diabetes Patients (T2D) 2024
Combination therapy with dapagliflozin plus exenatide leads to superior and sustained improvement in beta cell function (DI) compared to either drug alone. These data suggest that combination therapy with GLP-1 RA plus SGLT2i may enhance long-term preservation of beta-cell function in T2D patients.
Synergistic Effects of Dapagliflozin and Tirzepatide Combination Treatment on Weight Loss and Glucose Regulation in Diet-Induced Obese Animals 2024
The addition of dapagliflozin to tirzepatide resulted in further weight reduction and improvement in glycemic control compared to each drug alone.
SGLT2 Inhibitors and Parkinson’s Disease (PD) Risk in Older Populations with Type 2 Diabetes (T2D) 2024
In the Cox model (Figure), the SGLT2 inhibitor group was associated with a significantly lower risk of incident PD (HR 0.70 [95% CI 0.55-0.89]) than the DPP4 inhibitor group. The risk reduction of PD was particularly profound in non-Hispanic Black individuals (HR 0.24 [95% CI 0.07-0.86]) and insulin users (HR 0.49 [95% CI 0.32-0.77]).
Sodium–Glucose Cotransporter 2 Inhibitor Use and Risk of Dementia and Parkinson’s disease among Patients with Type 2 Diabetes—A Longitudinal, Nationwide, Population-Based Cohort Study 2024
Overall, use of SGLT2i was associated with a 22% lower risk for the composite of dementia from any cause and PD than use of other OADs (adjusted HR [aHR], 0.78 [95% CI 0.73─0.83]) with a 6-month lag period. Regarding the individual endpoints, SGLT2i use was associated with reduced risks for AD (aHR, 0.81 [95% CI 0.76─0.87]), VaD (aHR, 0.69 [95% CI 0.60─0.78]), and PD (aHR, 0.80 [95% CI 0.69─0.91]). In this nationwide population-based cohort study, SGLT2i use significantly reduced the risks for dementia and PD in patients with type 2 diabetes independent of various factors including comorbidities and bioclinical parameters.
Sotagliflozin vs. Empagliflozin or Placebo in Type 2 Diabetes on a DPP-4i +/- Metformin 2024
=> Sotagliflozin (SGLT1+2 inhibitor) is not better than empagliflozin (SGLT2i only) for HbA1c and other metabolic measurements.
Effects of empagliflozin on reproductive system in men without diabetes 2024
After one month of empagliflozin, there were no discernible changes in androgen, pituitary gonadotropin hormones, or inhibin B. Regardless of BMI category, the administration of empagliflozin, a highly selective SGLT2 inhibitor, did not alter serum androgen levels in men without diabetes. While SGLT2 is present in the testes, its inhibition does not seem to affect testosterone production in Leydig cells nor inhibin B secretion by the Sertoli cells.
(SGTL2i and cancer @Neo =>)
Sodium–glucose cotransporter 2 inhibitors and the cancer patient: from diabetes to cardioprotection and beyond 2024
This review will cover biological foundations and clinical evidence for SGLT2i modulating myocardial function and metabolism, with a focus on their possible use as cardioprotective agents in the cardio-oncology settings. Furthermore, we will explore recently emerged SGLT2i effects on hematopoiesis and immune system, carrying the potential of attenuating tumor growth and chemotherapy-induced cytopenias.
