INCREASED INSULIN BINDING BY LYMPHOCYTE RECEPTORS INDUCED BY Β-Oh BUTYRATE

Merimee, Thomas J.; Pulkkinen, Andrea J.; Lofton, Steven A

doi:10.1210/jcem-43-5-1190

Cited by 16 publications

(12 citation statements)

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“…Several workers reported results similar to our findings (Hidaka et al, 1981, Merimee et al, 1976 . Similar results were also obtained when soluble insulin receptors were substituted for adipocytes, suggesting that OHbutyrate has the potency to increase the insulin binding activity at the receptor level.…”

Section: Discussionsupporting

confidence: 92%

“…Several workers have studied the effects of ketone bodies and low pH on insulin binding to its receptor and on biochemical actions induced by insulin in target cells. Although it is reported that low pH not only reduces insulin binding (Shafie et al, 1979, Waelbroek, 1982, Sorge and Hilf, 1972 but also decreases the activity of insulin action subsequent to the binding of insulin to its receptor (Hidaka et al, 1981, Sonne et al, 1981, the effect of ketone bodies on the insulin binding is controversial (Van Putten el al., 1985, Merimee et al, 1976.…”

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confidence: 99%

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Effects of BETA-Hydroxy Butyric Acid on Insulin Binding to its Receptor and on Autophosphorylation of the Receptor.

et al. 1990

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We examined the effects of beta-hydroxy butyric acid (B-OH-butyrate) on insulin binding to its receptor and on autophosphorylation of the receptor in vitro. The affinity of isolated rat adipocyte insulin receptors was significantly increased by B-OH-butyrate at neutral pH. Similar results were obtained with soluble insulin receptors prepared from hepatocytes. Autophosphorylation of insulin receptor, however, was not affected by OH-butyrate at neutral pH.These results seggestd insulin resistance in ketoacidosis is not caused by an interaction between B-OH-butyrate and the insulin receptor.

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Section: Discussionsupporting

confidence: 92%

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confidence: 99%

Effects of BETA-Hydroxy Butyric Acid on Insulin Binding to its Receptor and on Autophosphorylation of the Receptor.

et al. 1990

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“…As indicated in Tables II and III, we have been unable to confirm this observation despite a wide variety of experimental conditions, including the identical conditions used by Merimee et al (33). No explanation for this difference is apparent.…”

Section: Discussioncontrasting

confidence: 54%

“…It seems possible that some small molecule (substrate or hormone), affected by fasting, could mediate this change, and Merimee et al (33) have recently reported that when cultured IM-9 lymphocytes are acutely exposed to 8-hydroxybutyrate, insulin binding increases. As indicated in Tables II and III, we have been unable to confirm this observation despite a wide variety of experimental conditions, including the identical conditions used by Merimee et al (33).…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of the Fasting-Induced Increase in Insulin Binding to Rat Adipocytes

Olefsky¹,

Kobayashi²

1978

J. Clin. Invest.

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A B S T R A C T Fasting leads to an increase in the ability ofadipocytes to bind insulin, and this was accounted for by an increase in the affinity ofthe receptors for insulin without any change in the number of receptors per cell. Binding affinity can increase because of a decrease in the dissociation rate constant (kd), an increase in the association rate constant (ka), or both. Kinetic studies demonstrated that fasting leads to a striking decrease in the rate at which insulin dissociates from its receptor, and the near two-fold prolongation of the time at which 50% of the bound 125I-insulin dissociates (28±4 vs. 50±5 min) correlated quite well with the two-fold increase in binding affinity. On the other hand, the rate at which insulin associates with its receptor was essentially unchanged. Negatively cooperative interactions between receptors were readily demonstrated in cells from control and fasting animals, and the magnitude and sensitivity ofthis effect was the same in both groups of cells. It seemed likely that during fasting a change in the concentration of some substrate or hormone could lead to these effects on insulin binding. However, in vitro attempts to recreate the substrate and hormonal changes which occur in fasting produced no evidence to support this idea. In conclusion: (a) fasting leads to an increase in the ability ofadipocytes to bind insulin because of an increase in binding affinity; (b) this increase in the affinity ofthe receptor for insulin was primarily accounted for by a decrease in the rate at which insulin dissociates from its receptors; and (c) fasting did not appreciably alter the negatively cooperative interactions displayed by adipocyte insulin receptors.

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“…1977). At the target cells, these factors might be responsible either directly or indirectly for impaired insulin receptor binding and inhibition of post-binding signals to intracellular effectors (Merimee et al 1976;Shafie et al 1979;Waelbroeck 1982;Van Putten et al 1985). However, the precise mechanism of insulin resistance in this condition is still obscure.…”

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confidence: 99%

Effect of Acidosis on Insulin Binding and Glucose Uptake in Isolated Rat Adipocytes.

Inamori

Yamatani

Fukase

et al. 1993

Tohoku J. Exp. Med.

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A., TOMINAGA, M. and SASAKI, H. Effect of Acidosis on Insulin Binding and Glucose Uptake in Isolated Rat Adipocytes. Tohoku J. Exp. Med., 1993, 169 (3), 205-213 To assess the mechanism of insulin resistance in metabolic acidosis, we investigated insulin receptor binding and glucose uptake in isolated rat epididymal adipocytes at three pHs, acidic (pH 6.8), neutral (pH 7.4) and alkaline (pH 8.0) groups. After male Sprague-Dawley rats weighing 220-240 g were submitted under chloral hydrate anesthesia, epididymal fat pads were dissected and isolated. [12511-insulin binding rate was not different between alkaline and neutral groups, but that of acidic group was markedly decreased to approximately 30% of neutral group at maximum specific insulin binding rate. Scatchard analysis showed that numbers of insulin receptors were not different among three groups, but values of binding affinity in acidic group was significantly lower than those of the others. 2-[3H]deoxy-D-glucose uptake of alkaline and neutral groups were increased to reach steady state immediately, but that of acidic group increased slowly and reached at maximum which was lower than the other two groups. Furthermore, 2-deoxy-D-glucose uptake against amount of bound insulin was lower in acidic group than other two groups. From these results, it is suggested that insulin resistance in metabolic acidosis resulted from the combined defects in binding affinity and post-binding process in the insulin receptor. insulin resistance ; acidosis ; insulin receptor ; glucose uptake ; adipocyte

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INCREASED INSULIN BINDING BY LYMPHOCYTE RECEPTORS INDUCED BY Β-Oh BUTYRATE

Cited by 16 publications

References 0 publications

Effects of BETA-Hydroxy Butyric Acid on Insulin Binding to its Receptor and on Autophosphorylation of the Receptor.

Effects of BETA-Hydroxy Butyric Acid on Insulin Binding to its Receptor and on Autophosphorylation of the Receptor.

Mechanisms of the Fasting-Induced Increase in Insulin Binding to Rat Adipocytes

Effect of Acidosis on Insulin Binding and Glucose Uptake in Isolated Rat Adipocytes.

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