The effect of streptozotocin-induced diabetes on phenylalanine hydroxylase expression in rat liver

Taylor, Daniel M.; Dahl, Hans Henrik M.; Mercer, Julian F. B.; Green, A K; Fisher, Michael J.

doi:10.1042/bj2640185

Cited by 11 publications

(3 citation statements)

References 42 publications

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“…The most important of these, gestational age, has been excluded by subgroup analysis. The effect of exogenous insulin on phenylalanine hydroxylase has not been proposed in preterm infants previously, although animal studies indicate it is biologically plausible 17 , 18 . Previous studies measuring preterm AA levels have not provided any insulin data 5 , 8 , 21 …”

Section: Discussionmentioning

confidence: 99%

“…Phenylalanine hydroxylase activity is increased in response to increased substrate provision, 14 although elevation of phenylalanine levels may occur 15 . Phenylalanine hydroxylase activity is also increased by steroid treatment 16 and reduced by insulin administration 17 , 18 in animal models. Both these drugs are used routinely in neonatal practice.…”

Section: Introductionmentioning

confidence: 99%

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Effect of Hyperalimentation and Insulin‐Treated Hyperglycemia on Tyrosine Levels in Very Preterm Infants Receiving Parenteral Nutrition

Mayes

Tan

Morgan

2012

J Parenter Enteral Nutr

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effect of Hyperalimentation and Insulin‐Treated Hyperglycemia on Tyrosine Levels in Very Preterm Infants Receiving Parenteral Nutrition

Mayes

Tan

Morgan

2012

J Parenter Enteral Nutr

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“…In order to achieve this, we generated a new line of transgenic mice overexpressing rat GK cDNA under control of the liver-specific human phenylalanine hydroxylase (PAH) gene promoter [18]. This promoter was chosen to direct expression of the GK transgene in the liver of IR -/-pups since it was shown to be expressed from late embryonic stages and to remain active under diabetic conditions [18,19].…”

mentioning

confidence: 99%

Improved metabolic disorders of insulin receptor-deficient mice by transgenic overexpression of glucokinase in the liver

et al. 2002

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Aims/hypothesis. Insulin receptor null mutant mice develop severe diabetes, ketoacidosis and liver steatosis and die within 1 week after birth. Since the liver plays an essential role in the control of glucose homeostasis, we examined in this work whether the metabolic disorders of insulin receptor-deficient mice could be improved upon restoration of hepatic glucose metabolism by transgenic constitutive overexpression of glucokinase selectively in the liver. Methods. We first generated transgenic mice overexpressing rat glucokinase cDNA under control of the liver-specific phenylalanine hydroxylase gene promoter. These transgenic mice were crossed with heterozygous insulin-receptor-null mutants to produce homozygous insulin-receptor-null mice overexpressing glucokinase in the liver. Results. The transgenic mice overexpressing glucokinase in the liver showed improved glucose tolerance and were mildly hypoglycaemic and hyperlipidaemic under starved conditions. The introduction of the glucokinase transgene in insulin receptor null mice did not prevent the development of glycosuria. However, ketoacidosis was delayed by more than 1 week and survival was prolonged to 10 to 16 days in 16% of the pups. In these longer surviving pups, serum glucose and triglyceride concentrations were lowered, hepatic glycogen stores were reconstituted and liver steatosis was absent as compared with the pups which had developed strong ketoacidosis and died earlier.Conclusions/interpretation. These results show that overexpression of hepatic glucokinase can compensate, in part, for the metabolic disorders developed by insulin receptor-deficient mice. This shows the importance of improving hepatic function in diabetes and must revive interest in enhancement of glucokinase activity as a therapeutic strategy for the treatment of diabetes. [Diabetologia (2002[Diabetologia ( ) 45:1292[Diabetologia ( -1297

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Differential expression of liver proteins in streptozotocin-induced diabetic rats in response to hypoglycemic mushroom polysaccharides

Hwang

Kim

Baek

et al. 2008

Korean J. Chem. Eng.

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We investigated the influence of hypoglycemic fungal extracellular polysaccharides (EPS) on the differential expression of liver proteins in streptozotocin (STZ)-induced diabetic rats. The results of diabetic study revealed that orally administrated EPS exhibited an excellent hypoglycemic effect, lowering the average plasma glucose level in EPS-fed rats to 55.1% with enhanced glucose tolerance. In the next step, we analyzed the differential expression patterns of rat liver proteins from each group to discover potent candidates for diabetes-associated proteins. 34 proteins were upregulated and 35 proteins were downregulated upon diabetes induction. Surprisingly, the altered levels of most proteins in the diabetic group were fully or partially restored to those of the non-diabetic control group by EPS treatment. Although the molecular basis of protein modulation after EPS administration in diabetic rats was not verified, the results of the proteomic analysis provide impetus for further studies to identify reliable biomarkers for diabetic therapy.

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The effect of streptozotocin-induced diabetes on phenylalanine hydroxylase expression in rat liver

Cited by 11 publications

References 42 publications

Effect of Hyperalimentation and Insulin‐Treated Hyperglycemia on Tyrosine Levels in Very Preterm Infants Receiving Parenteral Nutrition

Effect of Hyperalimentation and Insulin‐Treated Hyperglycemia on Tyrosine Levels in Very Preterm Infants Receiving Parenteral Nutrition

Improved metabolic disorders of insulin receptor-deficient mice by transgenic overexpression of glucokinase in the liver

Differential expression of liver proteins in streptozotocin-induced diabetic rats in response to hypoglycemic mushroom polysaccharides

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