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Keywords: glycemia, hepatocyte, hybrid, lactic acidosis, malate-aspartate shuttle, mitochondria, nitric oxide synthase, oxaloacetate, redox, tricarboxylic acid cycle Introduction Type 2 diabetes mellitus (T2DM) is characterized by carbohydrate, lipid, and protein metabolism dysregulation due to impaired insulin secretion and insulin resistance.1 In 2021, approximately 483 million people were diagnosed with T2DM globally, representing 9.45% of the population,2 and it remains a leading cause of mortality, claiming over a million lives each year.3 Currently, metformin is the first-line standard treatment for T2DM and the most common glucose-lowering medication,4 with more than 200 million patients using it daily.4 Metformin decreases both basal and postprandial plasma glucose levels.5 The glucose-lowering effects of metformin are mediated by increasing skeletal muscle glucose uptake and utilization,6 lowering intestinal carbohydrate absorption,6 and suppressing glucose production6 mainly by inhibiting hepatic gluconeogenesis,7,8 which is increased in T2DM.1 The activities of cytoplasmic enzymes that participate in gluconeogenesis are increased in rats with diabetes.9 Increased hepatic gluconeogenesis in T2DM is attributed to insulin resistance, insulin deficiency, hyperglucagonemia, increased glucagon sensitivity, and elevated substrate supply for gluconeogenesis.1 Animal studies indicate that nitric oxide (NO) supplementation has beneficial metabolic effects in T2DM by increasing insulin secretion10,11 (via increasing insulin synthesis and exocytosis,12 decreasing pancreatic islet oxidative stress,13 and increasing pancreatic islet blood flow10) and by stimulating peripheral glucose utilization (via increasing insulin sensitivity14 and increasing glucose uptake in skeletal muscle cells14 and adipocytes15)