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:1.1.1.49 (
glucose-6-phosphate dehydrogenase
)
7,794
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The effect of daily injections of T4, growth hormone and epidermal growth factor on the activities of the 3 hepatic enzymes malic enzyme (E.C.1.1.1.40), 6 phosphogluconate dehydrogenase (E.C.1.1.1.44) and
glucose 6-phosphate dehydrogenase
(E.C.1.1.1.49) in hypophysectomised rats was examined. T4 was shown to increase the activity of malic enzyme in a dose dependent manner from a basal level of 3.55 mumol/min/liver to 48.97 mumol/min/liver at a dose of 75 micrograms/Kg/day. A smaller increase in the activity of 6 phosphogluconate dehydrogenase was also observed over the same range of T4 dosage.
Growth hormone
in the current study increased the total liver enzyme activity of
glucose 6-phosphate dehydrogenase
by 84% when given with a replacement dose of 35 micrograms T4/kg/day and 6 phosphogluconate dehydrogenase activity by 19%.
...
PMID:The effects of chronic administration of T4, growth hormone and epidermal growth factor on hepatic lipogenic enzymes in hypophysectomised rats. 349 3
Triiodothyronine (T3) is involved in the regulation of the growth hormone-insulin-like growth factor I (GH-IGF-I) axis. In this study we investigated the effect of GH and IGF-I on the metabolic response of T3 in target tissues by evaluating the activity of two T3-dependent liver enzymes: mitochondrial alpha-glycerophosphate dehydrogenase (alpha-GPD) and cytosolic malic enzyme (ME) in rat hepatocytes in primary culture.
Growth hormone
(35 nmol/l) as well as IGF-I (0.5 mumol/l) reduced alpha-
GPD
and ME activities (p < 0.01) compared to the control group. Timecourse studies indicated that IGF-I (1.5 mumol/l) significantly decreased alpha-
GPD
and ME activities (P < 0.01) after 24 h, whereas the effect of GH (35 nmol/l) was recorded only after 36 h (p < 0.01). This delayed effect of GH compared to IGF-I suggested the possibility that the effect of GH could be mediated by IGF-I synthesis. To test this hypothesis, the effect of GH on the two enzyme activities was studied in the presence of anti-IGF-I antibodies. A gradual recovery of alpha-
GPD
and ME activities (p < 0.01) was observed in the presence of GH (35 nmol/l) plus increasing concentrations of anti-IGF-I antiserum. The maximal alpha-
GPD
and ME activities attained after the incubation of the liver cells with 1 mumol/l T3, a concentration high enough to fully saturate the nuclear T3 receptors for 24 h, were lowered significantly by 1.0 mumol/l IGF-I (p < 0.01). This finding suggests that the IGF-I effect might be independent of the saturation of the nuclear T3 receptors. In conclusion, in cultured rat hepatocytes, GH and IGF-I reduced the metabolic response of T3 evaluated by two liver T3-dependent enzyme activities. The effect of GH was mediated at least in part by IGF-I.
...
PMID:Response of triiodothyronine-dependent enzyme activities to insulin-like growth factor I and growth hormone in cultured rat hepatocytes. 863 May 22
Longitudinal growth is a result of proliferation and differentiation of chondrocytes in the growth plate.
Growth hormone
(GH) stimulates longitudinal growth, and GH receptors have been shown on growth plate chondrocytes, but the effects of GH on chondrocytes of different cell layers are not clear. To study the effect of GH on chondrocyte activity, in situ biochemical techniques were used to measure enzyme activities, which are associated with cell differentiation (alkaline phosphatase [ALP]) and osteoclast activity (tartrate-resistant acid phosphatase [TRAP]), within single cells of the growth plate. Uptake of bromodeoxyuridine (BrdU) was used as a parameter for proliferative activity. In addition,
glucose-6-phosphate dehydrogenase
(
G6PD
) was measured since increased proliferation has been associated with increased
G6PD
activity. The role of GH was studied in a model of isolated GH deficiency (dwarf rat) and complete pituitary deficiency (hypophysectomized rat). Groups of GH-deficient dwarf rats were infused with recombinant human GH in either a continuous or a pulsatile manner, since the pattern of GH secretion is an important regulator of growth in the rat. After 7 days,
G6PD
activity in proliferative chondrocytes and TRAP activity in osteoclasts was increased, while ALP activity in hypertrophic chondrocytes was decreased. GH not only increased the number of chondrocytes that incorporated BrdU but also the total number of chondrocytes in the proliferative zone; therefore, its ratio, the labeling index (an indicator of proliferative rate), was not increased. The widths of the proliferative and hypertrophic zones were increased by both patterns of GH administration. The width of the resting zone was unaffected by continuous GH but decreased by pulsatile GH. ALP and TRAP activities were, respectively, higher and lower in hypophysectomized rats compared with the GH-deficient animals. Hypophysectomized rats had smaller growth plates than dwarf rats with a disproportionally wide resting zone, which, like BrdU uptake, was not affected by GH. GH treatment resulted in increased TRAP and decreased ALP activity. These results indicate that GH stimulates the commitment of chondrocytes within the resting/germinal layer to a proliferative phenotype (as opposed to stimulating the rate of chondrocyte proliferation) but only in the presence of other pituitary hormones. Furthermore, this study shows that enzyme activities within single chondrocytes and osteoclasts are GH-sensitive. The extent to which these effects are direct or mediated by systemic or local growth factors remains to be clarified.
...
PMID:Single cell enzyme activity and proliferation in the growth plate: effects of growth hormone. 885 46
1. The concentration and oxidoreduction state of the liver nicotinamide nucleotides of rats subjected to a number of hormonal treatments have been measured. 2. Adrenalectomy decreases the NADP(+) content by 80% but has little effect on NAD(+), NADH or NADPH. High doses of cortisone produce similar changes, but more physiological doses (5mug. daily) tend to increase the NADP(+) content. 3. Glucagon treatment of normal rats lowered the NADH and NADP(+) concentrations but did not affect the total amounts present.
Growth hormone
increased the concentrations and total amounts of NAD(+) and NADH but significantly decreased the concentrations and total amounts of NADP(+) and NADPH. 4. Measurements have been made of a number of enzymes in the livers of adrenalectomized and glucagon-treated rats that could affect the oxidoreduction state of NADP. The activities of
glucose 6-phosphate dehydrogenase
and 6-phosphogluconate dehydrogenase are not affected by adrenalectomy or treatment with cortisone or glucagon. Nor does adrenalectomy affect the activity of NADPH-cytochrome c oxidoreductase or NADPH-glutathione oxidoreductase. The hepatic content of glutathione is, however, decreased 50% by adrenalectomy. 5. Measurements of the oxidation of [1-(14)C]glucose and [6-(14)C]glucose by liver slices from adrenalectomized rats showed that glucose oxidation was substantially normal, although phenazine methosulphate caused a smaller stimulation of the oxidation of C-1 of [1-(14)C]glucose in slices from the livers of adrenalectomized rats than it did with slices from controls. The hepatic synthesis of lipids from [1-(14)C]glucose was marginally increased in adrenalectomized rats. 6. The additional NADP(+) found when liver is extracted with 0.02n-sulphuric acid-0.1m-sodium sulphate is less affected than the NADP(+) extracted with 0.1n-hydrochloric acid in adrenalectomized or glucagon-treated rats. Hooded Norway rats appear to have less of this extra form of NADP(+) than albino rats. 7. An attempt has been made to correlate the observed changes in the nicotinamide nucleotides with metabolic patterns prevailing in different hormonal conditions.
...
PMID:THE EFFECT OF DIFFERENT HORMONAL CONDITIONS ON THE CONCENTRATION AND OXIDOREDUCTION STATE OF THE NICOTINAMIDE NUCLEOTIDES OF RAT LIVER. 1433 53
Silver sea bream, Sparus sarba, were fed two diets of different carbohydrate levels (2 and 20% dextrin) for 4 weeks, and the effects on organ indices, liver composition, serum metabolite and hormone levels and gene expression profile of key enzymes of carbohydrate metabolism in the liver were investigated. By using real-time PCR, mRNA expression levels of carbohydrate metabolic enzymes including glucokinase (GK, glycolysis), glucose-6-phosphatase (G6Pase, gluconeogenesis), glycogen synthase (GS, glycogenesis), glycogen phosphorylase (GP, glycogenolysis) and
glucose-6-phosphate dehydrogenase
(
G6PDH
, pentose phosphate pathway) in liver of sea bream have been examined, and it was found that high dietary carbohydrate level increased mRNA level of GK but decreased mRNA levels of G6Pase and GP. However, mRNA levels of GS and
G6PDH
were not significantly influenced by dietary carbohydrate. Silver sea bream fed high dietary carbohydrate had higher hepatosomatic index (HSI), liver glycogen and protein, but there were no significant changes in gonadosomatic index (GSI), serum glucose and protein level, as well as liver lipid and moisture level.
Pituitary growth hormone
(GH) and hepatic insulin-like growth factor I (IGF-I) transcript abundance were assayed by real-time PCR, and it was found that both parameters remained unchanged in fish fed different dietary carbohydrate levels. Serum triiodothyronine (T(3)) and thyroxine (T(4)) were not significantly affected by dietary carbohydrate levels, but lower serum cortisol level was found in fish fed high dietary carbohydrate level. These results suggest that silver sea bream is able to adapt to a diet with high carbohydrate content (up to 20% dextrin), the consumption of which would lead to fundamental re-organization of carbohydrate metabolism resulting in hepatic glycogen deposition.
...
PMID:Influence of dietary carbohydrate level on endocrine status and hepatic carbohydrate metabolism in the marine fish Sparus sarba. 2170 19
Growth hormone
(GH) transgenic salmon possesses markedly increased metabolic rate, appetite, and feed conversion efficiency, as well as an increased ability to compete for food resources. Thus, the ability of GH-transgenic fish to withstand periods of food deprivation as occurs in nature is potentially different than that of nontransgenic fish. However, the physiological and genetic effects of transgenic GH production over long periods of food deprivation remain largely unknown. Here, GH-transgenic coho salmon (Oncorhynchus kisutch) and nontransgenic, wild-type coho salmon were subjected to a 3-month food deprivation trial, during which time performance characteristics related to growth were measured along with proximate compositions. To examine potential genetic effects of GH-transgenesis on long-term food deprivation, a group of genes related to muscle development and liver metabolism was selected for quantitative PCR analysis. Results showed that GH-transgenic fish lose weight at an increased rate compared to wild-type even though proximate compositions remained relatively similar between the groups. A total of nine genes related to muscle physiology (cathepsin, cee, insulin-like growth factor, myostatin, murf-1, myosin, myogenin, proteasome delta, tumor necrosis factor) and five genes related to liver metabolism (carnitine palmitoyltransferase, fatty acid synthase, glucose-6-phosphatase,
glucose-6-phosphate dehydrogenase
, glucokinase) were shown to be differentially regulated between GH-transgenic and wild-type coho salmon over time. These genetic and physiological responses assist in identifying differences between GH-transgenic and wild-type salmon in relation to fitness effects arising from elevated growth hormone during periods of long-term food shortage.
...
PMID:Food Shortage Causes Differential Effects on Body Composition and Tissue-Specific Gene Expression in Salmon Modified for Increased Growth Hormone Production. 2626 85