Journal of Yeungnam Medical Science

Case Report

Metformin induced acute pancreatitis and lactic acidosis in a patient on hemodialysis.: Yeon Kyung Lee, Kihyun Lim, Su Hyun Hwang, Young Hwan Ahn, Gyu Tae Shin, Heungsoo Kim, In Whee Park; Yeungnam Univ J Med. 2016;33(1):33-36. Published online June 30, 2016; DOI: https://doi.org/10.12701/yujm.2016.33.1.33

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Metformin, commonly prescribed for type 2 diabetes, is considered safe with minimal side-effect. Acute pancreatitis is rare but potentially fatal adverse side-effect of metformin. We report a patient on hemodialysis with metformin-related acute pancreatitis and lactic acidosis. A 62-year-old woman with diabetic nephropathy and hypertension presented with nausea and vomiting for a few weeks, followed by epigastric pain. At home, the therapy of 500 mg/day metformin and 50 mg/day sitagliptin was continued, despite symptoms. Laboratory investigations showed metabolic acidosis with high levels of lactate, amylase at 520 U/L (range, 30-110 U/L), and lipase at 1,250 U/L (range, 23-300 U/L). Acute pancreatitis was confirmed by computed tomography. No recognized cause of acute pancreatitis was identified. Metformin was discontinued. Treatment with insulin and intravenous fluids resulted in normalized amylase, lipase, and lactate. When she was re-exposed to sitagliptin, no symptoms were reported.

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Sex-differences in [68Ga]Ga-DOTANOC biodistribution
A. Leisser, K. Lukic, M. Nejabat, W. Wadsak, M. Mitterhauser, M. Mayerhöfer, G. Karnaikas, M. Raderer, M. Hacker, A.R. Haug
Nuclear Medicine and Biology.2019; 76-77: 15. CrossRef

Review

Effects of AMP-activated Protein Kinase Activating Compounds and Its Mechanism.: Hyoung Chul Choi; Yeungnam Univ J Med. 2012;29(2):77-82. Published online December 31, 2012; DOI: https://doi.org/10.12701/yujm.2012.29.2.77

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Abstract PDF

AMP-activated protein kinase (AMPK) is an important cellular fuel sensor. Its activation requires phosphorylation at Thr-172, which resides in the activation loop of the alpha1 and alpha2 subunits. Several AMPK upstream kinases are capable of phosphorylating AMPK at Thr-172, including LKB1 and CaMKKbeta (Ca2+/calmodulin-dependent protein kinase kinasebeta). AMPK has been implicated in the regulation of physiological signals, such as in the inhibition of cholesterol fatty acid, and protein synthesis, and enhancement of glucose uptake and blood flow. AMPK activation also exhibits several salutary effects on the vascular function and improves vascular abnormalities. AMPK is modulated by numerous hormones and cytokines that regulate the energy balance in the whole body. These hormone and cytokines include leptin, adiponectin, ghrelin, and even thyroid hormones. Moreover, AMPK is activated by several drugs and xenobiotics. Some of these are in being clinically used to treat type 2 diabetes (e.g., metformin and thiazolidinediones), hypertension (e.g., nifedipine and losartan), and impaired blood flow (e.g., aspirin, statins, and cilostazol). I reviewed the precise mechanisms of the AMPK activation pathway and AMPK-modulating drugs.

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