Hormonal and dietary regulation of hepatic glucokinase

Sharma, C.B.; Manjeshwar, Rajani; Weinhouse, Sidney

doi:10.1016/s0065-2571(64)80013-3

Cited by 106 publications

(73 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Of particular relevance to the present study is the demonstration of hexokinase (14,16), glucokinase (14,16), and glucose-6-phosphatase (16, 17) activity in the beta cell. The temporal pattern for the disappearance and reappearance of insulin secretory responsiveness to glucose during starvation and refeeding is remarkably similar to that of hepatic glucokinase (18,19 Kipnis [23] and Luft [24]). These same individuals, however, may ex-hibit normal insulin secretory responses to other secretogogues which act closer to the terminal events of the secretory system.…”

Section: Discussionmentioning

confidence: 84%

The effect of fasting, diet, and actinomycin D on insulin secretion in the rat

Grey¹,

Goldring²,

Kipnis³

1970

J. Clin. Invest.

124

View full text Add to dashboard Cite

A B S T R A C T The present studies were performed to elucidate the mechanisms responsible for the impairment of glucose-stimulated insulin secretion observed in fasting. Rats fasted for 48 hr displayed marked impairment in their insulin secretory response to both oral and intravenous glucose. Glucose-stimulated insulin secretion was restored within 24 hr by refeeding; actinomycin D given before refeeding blocked the expected return of normal glucose-stimulated insulin secretion despite adequate food intake. Fasted rats refed a diet devoid of carbohydrate failed to display a return of normal insulin secretory responsiveness to oral glucose in contrast to rats fed isocalorically a high carbohydrate diet. Differences in insulin secretion in fed, fasted, and fasted-refed rats could not be attributed to changes in pancreatic insulin content. There was no significant difference in the insulin secretory response to aminophylline of fed, fasted, or fasted-refed rats. The intermittent pulsing of fasted rats with hyperglycemic episodes by the injection of small amounts of glucose (500 mg) intraperitoneally every 8 hr ameliorated the impairment of glucose-stimulated insulin secretion characteristic of the fasting state. These results suggest that the impairment of glucose-stimulated insulin secretion during fasting and its restoration by refeeding are regulated by changes in a glucose-inducible enzyme system in the pancreatic beta cell. INTRODUCTIONStarvation results in a decrease in the basal plasma insulin levels of all species thus far studied (1-4) and, where measured, in an impairment of glucose-stimulated

show abstract

Section: Discussionmentioning

confidence: 84%

The effect of fasting, diet, and actinomycin D on insulin secretion in the rat

Grey¹,

Goldring²,

Kipnis³

1970

J. Clin. Invest.

124

View full text Add to dashboard Cite

show abstract

“…Administration of triiodothyronine (1 .0 pg/g) restored activity to near the levels for normal untreated animals. .01 (4) Actinomycin D or puromycin reduced the precocious development of glucokinase caused by administration of triiodothyronine and glucose. Complete inhibition was observed with actinomycin D at a dose of 0.2 pg per g body wt in animals at both the 8th (Table 6) and 16th days.…”

Section: Resultsmentioning

confidence: 99%

“…Insulin, which controls glucokinase activity in the adult rat [4,18] produced no more than half the glucokinase activity observed with triiodothyronine and glucose induction when substituted for glucose. The effects of triiodothyronine and insulin were variable and showed no clear relationship to the dose of insulin.…”

Section: Discuss I 0 Nmentioning

confidence: 99%

See 1 more Smart Citation

Premature Induction of Glucokinase in the Neonatal Rat by Thyroid Hormone

Partridge

Hoh

Weaver

et al. 1975

European Journal of Biochemistry

View full text Add to dashboard Cite

It was shown that the development of liver glucokinase in the rat coincided with a peak in the levels of circulating thyroid hormone at about the 16th postnatal day. Administration of thyroid inhibitors blocked the development of the enzyme and administration of thyroid hormone restored activity to normal levels. Glucokinase could be induced prematurely as early as the 2nd postnatal day by the administration of thyroid hormone followed by daily injection of glucose (10 mg/g body weight). Glucocorticoids and corticotropin failed to induce glucokinase activity prematurely. The postnatal increase in circulating thyroid hormone levels together with increased intake of carbohydrate at weaning may be the normal physiological stimulus for induction of this enzyme.

show abstract

“…100 (159) 100 (4 h) (258) 141 (6 % CHO) (207) ND 100 (43 % CHO) (136) Fasted ND 46 (24 h) (159) † 37 (72 h) (258) 100 (259) ND ND High CHO 129 (21 % CHO) (211) 100 (38 % CHO) (162) 105 (100 % CHO) (62) 1200 (20 % CHO) (259) 108 (38 % CHO) (162) ND High fat ND ND 48 (6 % fat, 20 d) (82) 93 (26 % fat) (224) ‡ ND 41 (52 % fat) (136) High protein 20 (0 % CHO) (211) 94 (14 % CHO) (162) † 67 (90 % protein, 20 d) (82) 100 (0 % CHO) (259) 100 (14 % CHO) (162) ND Refed ND 56 (4 h), 100 (24 h) (62) 388 (6 % CHO, 1 week) (207) ND ND CHO tolerance test ND 201 (oral saccharose 3 g/kg) (163) 86 (oral glucose 3·6 g/kg)…”

Section: Rattus Norvegicusmentioning

confidence: 99%

Nutritional regulation of glucokinase: a cross-species story

Panserat

Rideau²,

Polakof

2014

Nutr. Res. Rev.

View full text Add to dashboard Cite

The glucokinase (GK) enzyme (EC 2.7.1.1.) is essential for the use of dietary glucose because it is the first enzyme to phosphorylate glucose in excess in different key tissues such as the pancreas and liver. The objective of the present review is not to fully describe the biochemical characteristics and the genetics of this enzyme but to detail its nutritional regulation in different vertebrates from fish to human. Indeed, the present review will describe the existence of the GK enzyme in different animal species that have naturally different levels of carbohydrate in their diets. Thus, some studies have been performed to analyse the nutritional regulation of the GK enzyme in humans and rodents (having high levels of dietary carbohydrates in their diets), in the chicken (moderate level of carbohydrates in its diet) and rainbow trout (no carbohydrate intake in its diet). All these data illustrate the nutritional importance of the GK enzyme irrespective of feeding habits, even in animals known to poorly use dietary carbohydrates (carnivorous species).

show abstract

Hormonal and dietary regulation of hepatic glucokinase

Cited by 106 publications

References 18 publications

The effect of fasting, diet, and actinomycin D on insulin secretion in the rat

The effect of fasting, diet, and actinomycin D on insulin secretion in the rat

Premature Induction of Glucokinase in the Neonatal Rat by Thyroid Hormone

Nutritional regulation of glucokinase: a cross-species story

Contact Info

Product

Resources

About