phosphoenolpyruvate has been researched along with Compensatory Hyperinsulinemia in 2 studies
Phosphoenolpyruvate: A monocarboxylic acid anion derived from selective deprotonation of the carboxy group of phosphoenolpyruvic acid. It is a metabolic intermediate in GLYCOLYSIS; GLUCONEOGENESIS; and other pathways.
phosphoenolpyruvate : A monocarboxylic acid anion resuting from selective deprotonation of the carboxy group of phosphoenolpyruvic acid.
phosphoenolpyruvic acid : A monocarboxylic acid that is acrylic acid substituted by a phosphonooxy group at position 2. It is a metabolic intermediate in pathways like glycolysis and gluconeogenesis.
Compensatory Hyperinsulinemia: A GLUCOSE-induced HYPERINSULINEMIA, a marker of insulin-resistant state. It is a mechanism to compensate for reduced sensitivity to insulin.
Excerpt | Relevance | Reference |
---|---|---|
"The principal response to hyperinsulinemia was a decrease in the recycling of OAA to lactate, because there was no significant change in the conversion of OAA to PEP." | 1.29 | Response of phosphoenolpyruvate cycle activity to fasting and to hyperinsulinemia in human subjects. ( Baba, H; Chinkes, D; Rosenblatt, J; Wolfe, RR; Zhang, XJ, 1996) |
Timeframe | Studies, this research(%) | All Research% |
---|---|---|
pre-1990 | 0 (0.00) | 18.7374 |
1990's | 1 (50.00) | 18.2507 |
2000's | 1 (50.00) | 29.6817 |
2010's | 0 (0.00) | 24.3611 |
2020's | 0 (0.00) | 2.80 |
Authors | Studies |
---|---|
Wolfe, RR | 1 |
Chinkes, D | 1 |
Baba, H | 1 |
Rosenblatt, J | 1 |
Zhang, XJ | 1 |
Edgerton, DS | 1 |
Cardin, S | 1 |
Emshwiller, M | 1 |
Neal, D | 1 |
Chandramouli, V | 1 |
Schumann, WC | 1 |
Landau, BR | 1 |
Rossetti, L | 1 |
Cherrington, AD | 1 |
2 other studies available for phosphoenolpyruvate and Compensatory Hyperinsulinemia
Article | Year |
---|---|
Response of phosphoenolpyruvate cycle activity to fasting and to hyperinsulinemia in human subjects.
Topics: Fasting; Humans; Hyperinsulinism; Lactic Acid; Male; Models, Biological; Oxaloacetates; Phosphoenolp | 1996 |
Small increases in insulin inhibit hepatic glucose production solely caused by an effect on glycogen metabolism.
Topics: Animals; Blood Glucose; Carbon Radioisotopes; Deuterium Oxide; Dogs; Female; Glucagon; Gluconeogenes | 2001 |