Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The rates of production of total ketone bodies (acetoacetate + beta-hydroxybutyrate) were determined using an isotope tracer technique in 23 obese subjects submitted to a fast of variable duration (15 hr--23 days). Constant infusions of 14C-acetoacetate were used in most studies, but similar results were obtained with pulse injections of this tracer or with constant infusions of 14C-D(-)-beta-hydroxybutyrate. Blood concentration, production rate, and urinary elimination of total ketones rose during approximately the first 3 days of fast and plateaued thereafter at values amounting, respectively, to 7.09 +/- 0.32 mumole/ml, 1908 +/- 80 mumole/min and 167 +/- 14 mumole/min. The rates of ketogenesis are significantly higher than those usually reported in the literature. Ketonemia was an exponential function of production rate suggesting that tissue uptake becomes progressively saturated as inflow rate rises. The same type of relationship between concentration and inflow rate was observed in nine control overnight fasted obese subjects rendered hyperketonemic with infusions of variable amounts of unlabeled acetoacetate. The comparison between the fasted and the control subjects at ketone concentrations of 3--10 mumole/ml showed that on an average, starvation is associated with a 35% decrease in the metabolic clearance rate of ketones. These data suggest that fasting is associated with an impairment of mechanisms for utilizing ketones, this defect contributing to the hyperketonemia of food deprivation.
 ...
PMID:Kinetics of ketone body metabolism in fasting humans. 75 25

Ketonaemia is well documented as a consequence of prolonged starvation, acute alcoholism, and uncontrolled diabetes mellitus. However, its occurrence in acute pancreatitis has not been described. In this report, three patients who manifested ketoacidosis at the time of presentation of acute pancreatitis are described. In none of these patients could ketoacidosis be attributed to any of the well known pathogenetic factors such as ethanol, diabetes mellitus or prolonged starvation. In one patient, both the serum ketone titres and increased anion gap persisted for several days during the recovery period, despite appropriate therapy (including restriction of oral intake or nasogastric suction, intravenous fluids, and analgesic administration), before declining in parallel with a decrease in serum lipase levels, and became undetectable following near normalisation of serum lipase. Therefore, we believe that pancreatic ketosis or ketoacidosis may be a distinct syndrome with ketogenesis being promoted and maintained by extremely high circulating pancreatic lipase concentrations.
 ...
PMID:Pancreatic ketoacidosis: ketonemia associated with acute pancreatitis. 770 90