Obesity is the primary cause of type 2 diabetes (T2D); Diabetes-related chronic heart failure is also a fatal complication of T2D. The central nervous system regulates feeding behavior and body weight in mammals via several neuroendocrine pathways

as well as many physiological processes related to energy consumption. Numerous studies have linked obesity's onset and progression to endocrine regulation disorders in the central nervous system. As a result

diabetic remission can be achieved in the early onset of T2D using a combination of diet

exercise

and medications. Obesity intervention can delay type 2 diabetes onset and complications. New antidiabetic drugs frequently used in endocrinology

such as glucagon-like peptide-1 receptor agonist (GLP-1RA) and sodium-glucose cotransporter-2 inhibitor (SGLT-2i)

have been observed to improve obesity and cardiovascular issues. GLP-1RA could reduce 26% of the cardiovascular complication; SGLT2i can reduce chronic heart failure by 30% in diabetic patients. There are two questions still puzzle clinicians:1. Whether GLP-1RA transport can across the blood-brain barrier (BBB)

and in which nuclei does it control diet and energy balance？2. Whether SGLT2i can transport across the BBB and inhibit the over-activated sympathetic nervous system

thereby reducing heart rate and inhibiting chronic heart failure？Therefore

this article summarizes the possible central nervous system pathways and mechanisms of these two drugs to control diet and reduce heart failure.