Please help explain with possible mechanisms with references for a better understanding.
Dear Joseph Chimezie
I wish all the best for you. You inserted an interesting question there. Please kindly note that for each term you mentioned in this question there are some good review papers that can help you for a better understanding of the given matters. Please kindly check the following papers:
1. https://pubmed.ncbi.nlm.nih.gov/27097605/
2. https://www.mayoclinic.org/diseases-conditions/hyperglycemia/symptoms-causes/syc-20373631
3. https://journals.sagepub.com/doi/abs/10.1177/2150135120903977?journalCode=pcha
Ketosis results from restriction of carbohydrate usage with increased reliance on fat oxidation for energy production. The pathogenesis of diabetic ketoacidosis (DKA) is well established (1). Briefly, absolute insulin deficiency leads to reduced glucose utilization and enhanced lipolysis; increased delivery of free fatty acids (FFAs) to the liver coupled with raised glucagon levels promotes FFA oxidation and production of ketone bodies. In both T1D and T2D, DKA presents with marked hyperglycemia (>250 mg/dL, typically 350–800 mg/dL), profuse glycosuria (2–4 mg ⋅ min−1 ⋅ kg−1), and hyperketonemia (plasma β-hydroxybutyrate 4.2–11.0 mmol/L) (2,3). The hyperglycemia of DKA is associated with extreme insulin resistance, manifesting itself as markedly (>70%) reduced tissue glucose disposal and increased endogenous glucose production (EGP) (3).
1 . Kitabchi AE, Umpierrez GE, Murphy MB. Diabetic ketoacidosis and hyperosmolar state. In International Textbook of Diabetes Mellitus. 4th ed. DeFronzo RA, Ferrannini E, Zimmet P, Alberti KGMM, Eds. New York, John Wiley & Sons, Ltd., 2015, p. 799–814.
2. Barrett EJ, DeFronzo RA, Bevilacqua S, Ferrannini E. Insulin resistance in diabetic ketoacidosis. Diabetes 1982;31:923–928.
3.Luzi L, Barrett EJ, Groop LC, Ferrannini E, DeFronzo RA. Metabolic effects of low-dose insulin therapy on glucose metabolism in diabetic ketoacidosis. Diabetes 1988;37:1470–1477
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