Figure 2.

Schematic description of the potential factors involved in fasting-associated diuresis and natriuresis and their disappearance post-prandially in normoglycemic obese hypertensive subjects as compared with diabetic patients. Fasting natriuresis and post-prandial-induced antidiuresis are prominent especially among hypertensive patients. While glucagon, natriuretic peptides, and ketones have been suggested as mediators of fasting natriuresis, insulin and the activation of the renin–angiotensin–aldosterone (RAAS) system and the sympathetic nervous system (SNS) were suggested to enhance post-feeding sodium retention. At the tubular levels, fasting is associated with a reduced proximal tubular sodium uptake, mediated by an impaired SGLT-2 activity, whereas the opposite takes place post-prandially. The latter phenomenon might be more pronounced in diabetics due to prolonged post-prandial hyperglycemia and intense SGLT-driven transport.