Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: EC:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hexokinase II (HKII) is the predominant hexokinase isozyme expressed in insulin-responsive tissues. Since defects involving glucose transport and/or its phosphorylation to glucose-6-phosphate are present in muscle of insulin-resistant humans, HKII should be viewed as a candidate gene for inherited insulin resistance and susceptibility to non-insulin-dependent diabetes mellitus (NIDDM). To investigate the prevalence of potential mutations in the gene encoding HKII, we used the polymerase chain reaction (PCR) to amplify each of the 18 exons of the HKII gene from genomic DNA derived from 59 subjects: 25 insulin-resistant probands with clinical features of the type A syndrome and 34 NIDDM subjects enrolled in the United Kingdom Prospective Study of Therapies of NIDDM (UKPDS) who represented the highest percentile of fasting hyperinsulinemia in the UKPDS population of 5,098 subjects. PCR products corresponding to individual HKII exons derived from each subject were screened for the presence of nucleotide variation using a sensitive nonradioactive single-strand conformation polymorphism (SSCP) protocol. Variant SSCP patterns indicative of genetic variation were detected only in PCR amplimers containing exons 4-7, 10, 15, and 17. Direct sequencing of amplified DNA from individuals affected with variant SSCP patterns revealed the presence of the following silent polymorphisms: Asp251 (GAT/C) in exon 7 and Asn692 (AAT/C) in exon 15. SSCP variants detected in PCR products containing exons 5, 10, and 17 were due to single base substitutions in flanking intronic sequences. A polymorphic GGA repeat was identified within intron 5.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Analysis of the hexokinase II gene in subjects with insulin resistance and NIDDM and detection of a Gln142-->His substitution. 788 22

ZF-L cells were derived from normal adult zebrafish liver, and have been growing in culture for more than 100 generations. The cells were derived in basal nutrient medium supplemented with fetal bovine serum (FBS), trout serum, trout embryo extract, bovine insulin and mouse epidermal growth factor. After 50 generations in culture, optimal growth of the cells was achieved in medium supplemented with FBS (5%) and trout serum (0.5%). ZF-L cells were hypodiploid (modal chromosome number = 46) and exhibited an epithelial morphology. ZF-L cell homogenates exhibited alanine and aspartate aminotransferase, glucose-6-phosphatase and alkaline phosphatase enzyme activities. The cells synthesized and released several proteins into the culture medium, including a 70 kDa protein recognized by anti-bovine serum albumin IgG.
...
PMID:Derivation and characterization of a zebrafish liver cell line. 799 34

A beef cow was examined to find the cause of decreasing appetite of 2 weeks' duration. The cow was obese (body condition score, 8 of 9), and multiple fetuses were identified on palpation per rectum. Urinalysis revealed > 160 mg of ketones/dl. Abnormal serum biochemical data included high concentrations of bilirubin, creatinine, sodium, and chloride; low concentrations of total CO2 and calcium; and high activity of aspartate transaminase. Treatment included administration of dextrose solution, i.v.; propylene glycol, PO; and insulin, i.v. and SC. The cow's appetite improved gradually over 8 days of treatment. Concentration of ketone bodies in urine decreased to trace amounts by day 4. The cow was discharged on day 10 and gave birth to twins 4 days after discharge (duration of gestation, 279 days). The clinical history of this cow differed from the history of other cattle with ketosis, but mimicked pregnancy toxemia in ewes. Multiple fetuses have not been implicated as a predisposing factor in severe prepartum ketosis of cows.
...
PMID:Severe prepartum ketosis in an obese beef cow. 784 49

Triiodothyronine (T3) treatment of pregnant rats for 6 days, 10 micrograms/100 g, resulted in a pronounced induction of enzymes related to gluconeogenesis and lipogenesis and of mitochondrial FAD-glycerophosphate dehydrogenase in the maternal liver, as previously observed in male rats. There was virtually no change in the activity of these enzymes in the placenta. However, there was a distinct induction of these enzymes in the fetal liver, even if increments in fetal serum and liver T3 were much smaller than on the maternal side. This indicates that changes in hepatic enzyme activities are a more sensitive index of fetal hyperthyroidism than T3 levels. The increased lipogenic capacity was expressed by greater incorporation of a tritium tracer into fatty acids. Administration of triamcinolone, 2 mg/100 g, for the last 5 days of gestation resulted in marked induction of maternal hepatic enzymes of lipogenesis, gluconeogenesis and of aspartate aminotransferase (ASAT), known to occur in male rats, as well as in a metabolic pattern of insulin resistance. The response of placental enzymes was limited to a small elevation in ASAT and phosphoenolpyruvate carboxykinase (PEPCK) activity. In the fetal liver there was no stimulation of lipogenic enzymes, but a marked induction of PEPCK and ASAT. The changes in the lipogenic capacity were confirmed by tritium incorporation into serum and liver fatty acids. These results demonstrate the marked sensitivity of specific fetal enzyme systems to the maternal iatrogenic hyperthyroidism or hypercorticism. The limited alterations in placental enzyme activities are in accord with the concept that placental metabolic stability fulfils a protective function toward the fetus.
...
PMID:Modulation of fetal and placental metabolic pathways in response to maternal thyroid and glucocorticoid hormone excess. 813 95

Experimental diabetes was induced in 4 wethers of the Mutton Merino breed by intravenous injection of alloxan (75 mg.kg-1) in order to determine its impact on plasma glucose, immunoreactive insulin, free fatty acids (FFA), cholesterol, phospholipids, triglycerides, D-(-)-3-hydroxybutyrate (D-3-HB), bilirubin and aspartate aminotransferase (ASAT) as well as on the changes of these parameters brought about by an intravenous infusion of sodium n-butyrate (1 mmol.kg-1). Alloxan administration caused a significant elevation of plasma glucose, FFA, triglycerides, cholesterol, phospholipids, D-3-HB and bilirubin and a decrease of the level of immunoreactive insulin. The increase in glucose level brought about by a bolus injection of sodium n-butyrate in untreated sheep did not appear in alloxanized animals. Thus, it is suggested that the lack of hyperglycaemic response in diabetic sheep was due to the absence of liver glycogen stores. Unexpectedly in alloxan-diabetic sheep, a decrease in the plasma level of FFA occurred after the administration of sodium n-butyrate. Therefore, it may be assumed that beside insulin other factors may contribute to the decrease of FFA under these conditions.
...
PMID:Acute metabolic and hormonal effects of intravenously administered sodium n-butyrate in untreated and alloxan-diabetic sheep. 821 52

Glurenorm, a IInd generation sulfanylurea preparation, was used for a year as a sugar-reducing drug in 20 patients with non-insulin-dependent diabetes mellitus and concomitant diseases of the liver (cirrhosis, chronic hepatitis, n = 5) and biliferous duct (cholelithiasis, a state following cholecystectomy, chronic cholecystitis, n = 15). A year follow-up has not shown deterioration of liver function as indicated by results of liver tests (AST, ALT, acid phosphatase, gamma-glutamyltranspeptidase, bilirubin, cholesterol, triglycerides). The hypoglycemic effect of the drug proved to be inferior to that of sulfanylurea derivatives, but the absence of side effects permit higher doses of glurenorm (up to 4-6 tablets daily) as against other oral sugar-reducing drugs.
...
PMID:[Glurenorm in the treatment of patients with non-insulin-dependent diabetes mellitus with diseases of the liver and bile ducts]. 841 21

This study was conducted to determine whether the administration of tri-iodothyronine (T3) to brain-dead donor pigs would improve hemodynamic instability, serum levels of thyroid hormones, or the outcome of transplantation of donor livers. Brain death was caused in young pigs (25-38 kg) by rapid inflation of an intracranially implanted balloon catheter. The animals were maintained on a ventilator and frequent measurements of acid/base balance, electrolytes, and glucose were made. At the end of 16 hr, livers were removed and implanted into prepared recipients. Serum-free tri-iodothyronine fell to zero at the end of 16 hr, and there was a 4-6-fold decline in free thyroxine (T4). The levels of serum reverse T3 (rT3) however, increased up to 6-fold. In animals treated with tri-iodothyronine 2 micrograms/hr, the serum levels of free T3 and T4 were not changed but the levels of serum reverse T3 (rT3) increased further. There were no apparent correlations between any hemodynamic parameter and serum thyroid hormone levels in the donors. After the liver transplants, recipients could be divided into those that survived longer than 6 days and those that did not. Although there were significant differences in the plasma levels of alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase, there was no correlation between survival and whether the donor had received tri-iodothyronine. Although other hormones, including insulin and cortisol, may also be necessary, there is no indication from these studies that the administration of tri-iodothyronine to brain-dead donors of liver grafts benefits the serum hormone levels in the donors or the subsequent survival of the recipients.
...
PMID:The influence of thyroid hormone replacement in a porcine brain death model. 845 62

In islets from adult rats injected with streptozotocin during the neonatal period, both a nonmetabolized analog of L-leucine and 3-phenylpyruvate augmented 14CO2 output from islets either prelabeled with L-[U-14C]glutamine or exposed to D-[2-14C]glucose and D-[6-14C]glucose, in a manner qualitatively comparable to that found in islets from control rats. The islets of diabetic rats differed, however, from those of control rats by their unresponsiveness to both the L-leucine analog and a high concentration of D-glucose in terms of increasing 3HOH generation from [2-3H]glycerol, an impaired sparing action of the hexose upon 14CO2 output from islets prelabeled with [U-14C]palmitate, and, most importantly, by a decreased rate of D-[2-14C]glucose and D-[6-14C]glucose oxidation when either incubated at a high concentration of the hexose (16.7 mM) or stimulated by nonglucidic nutrient secretagogues at a low concentration of D-glucose (2.8 mM). In islet homogenates, the activity of glyceraldehyde phosphate dehydrogenase, glutamate decarboxylase, and NADP-malate dehydrogenase was lower in diabetic than control islets. Such was not the case for glutamate-alanine transaminase, glutamate-aspartate transaminase, or glutamate dehydrogenase. The neonatal injection of streptozotocin thus affected, in the adult rats, the activity of several islet enzymes. Nevertheless, the metabolic data suggest that an impaired circulation in the glycerol phosphate shuttle, as observed in response to stimulation of the islets by either a high concentration of D-glucose or nonglucidic nutrient secretagogues, represents an essential determinant of the preferential impairment of glucose-induced insulin release in this model of non-insulin-dependent diabetes.
...
PMID:Metabolic response to nonglucidic nutrient secretagogues and enzymatic activities in pancreatic islets of adult rats after neonatal streptozotocin administration. 848 60

Intravenous administration of 500 ml of 50% glucose solution to 10 nonketotic dairy cows increased the blood glucose and insulin concentrations 7-fold immediately following administration. Blood glucose and insulin concentrations of ketotic cows were about 6- and 3-fold higher, respectively, immediately following glucose administration. Administration of 1000 ml of 25% xylitol (xylo-pentane-1,2,3,4,5-pentol) in nonketotic cows increased blood glucose and insulin concentrations 2- and 9-fold, respectively. Ketotic cows treated with xylitol exhibited blood insulin concentration 12-fold higher following administration. This insulin increase might be explained by a decrease in insulin degradation because of the diffusion of xylitol, which is not dependent on insulin in peripheral tissues. For ketotic cows given xylitol, serum concentrations of free fatty acid decreased, and triglyceride concentrations and aspartic acid aminotransferase activity increased, but values were unchanged by xylitol administration to nonketotic cows. Thus, for ketotic cows, the responses of the blood glucose and insulin concentrations to xylitol administration were better than those responses to glucose administration. Improvements in clinical signs, i.e., disappearance of urinary ketone bodies and recovery to normal feed consumption, also suggested the usefulness of xylitol administration for the treatment of ketosis.
...
PMID:Glucose and xylitol tolerance tests for ketotic and healthy dairy cows. 870 96

There is strong evidence that genetic factors contribute to the development of obesity in humans as well as laboratory animals. Another important factor leading to obesity is an increase in energy intake. However, it is difficult to make normal rats obese by controlling daily food intake. There is no report of normal adult male Wistar rats becoming obese and diabetic on a high-fat diet. The aim of the present study was, therefore, to make normal adult Wistar rats obese by infusing high fat and hypercaloric diet through the cannula without disturbing the free movement and to investigate the influence of an increase in the caloric intake on body weight and glucose metabolism. High-fat hypercaloric diet (360 kcal/kg body wt./day; H group) or control diet (180 kcal/kg body wt./day; C group) was continuously infused into the stomach of normal adult male Wistar rats weighing approximately 300 g through gastric cannulas for 27 days. On day 28 after a 24-h fasting, serum concentrations of aspartate aminotransferase, alanine aminotransferase, total cholesterol, triglyceride, phospholipid, and free fatty acids (FFA) were determined, and intragastric glucose loading test (2 g/kg body wt.) was performed. The average weekly body weight gain in the H group was twice as much as that of the C group (40.0 +/- 2.4 vs. 19.4 +/- 1.9 g/week, P < 0.001). Serum levels of triglyceride, phospholipid, total cholesterol, and FFA were significantly elevated in the H group compared to those in the C group. Liver weight in the H group was significantly higher than that in the C group and showed steatosis. Pancreas weight (-13%) as well as protein (-12%), amylase (-53%) and trypsin content (-26%) were all reduced, whereas pancreatic DNA content was significantly increased in the H group compared to those in the C group. Serum glucose and insulin concentrations before and after glucose loading in the H group were significantly higher than those in the C group. Moreover, the insulin response relative to glucose response in the H group was significantly high compared to that in the C group, indicating the presence of insulin resistance. These results indicate that feeding of high-fat hypercaloric diet makes normal Wistar male adult rat obese associated with hyperlipidemia, hyperinsulinemia, and glucose intolerance.
...
PMID:High-fat hypercaloric diet induces obesity, glucose intolerance and hyperlipidemia in normal adult male Wistar rat. 879 99


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>

---