SGLT2 inhibition alters substrate utilization and mitochondrial redox in healthy and failing rat hearts.

Previous studies highlight the potential for sodium-glucose cotransporter type 2 (SGLT2) inhibitors (SGLT2i) to exert cardioprotective effects in heart failure by increasing plasma ketones and shifting myocardial fuel utilization toward ketone oxidation. However, SGLT2i have multiple in vivo effects and the differential impact of SGLT2i treatment and ketone supplementation on cardiac metabolism remains unclear. Here, using gas chromatography-mass spectrometry (GC-MS) and liquid chromatography-tandem mass spectrometry (LC-MS/MS) methodology combined with infusions of [13C6]glucose or [13C4]βOHB, we demonstrate that acute SGLT2 inhibition with dapagliflozin shifts relative rates of myocardial mitochondrial metabolism toward ketone oxidation, decreasing pyruvate oxidation with little effect on fatty acid oxidation in awake rats.

Effects of atrial fibrillation screening according to thyroid function: Post-hoc analysis of the randomized LOOP study.

Purpose: Subclinical thyroid dysfunction is a marker for atrial fibrillation (AF) and stroke risk. This study explored the effects of AF screening according to thyroid-stimulating hormone (TSH) levels.

Methods: An AF screening trial (the LOOP study) was analyzed post-hoc according to baseline TSH.

[Not Available].

This review summarises the current and possible future insulin treatment of type 2 diabetes. The type 2 diabetes treatment guidelines prioritise a person-centred approach with various options before insulin addressing cardiorenal protection. Long-acting daily insulin injections are warranted in severe hyperglycaemia or when glycaemic targets are not met.

Revisiting the role of glucagon in health, diabetes mellitus and other metabolic diseases.

Insulin and glucagon exert opposing effects on glucose metabolism and, consequently, pancreatic islet β-cells and α-cells are considered functional antagonists. The intra-islet hypothesis has previously dominated the understanding of glucagon secretion, stating that insulin acts to inhibit the release of glucagon. By contrast, glucagon is a potent stimulator of insulin secretion and has been used to test β-cell function.