Impaired insulin mediated potassium uptake in adolescents with IDDM

Arslanian, Silva; Austin, Audrey

doi:10.1016/0885-4505(91)90084-x

Cited by 9 publications

(8 citation statements)

References 27 publications

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“…DeFronzo et al studied 29 normal nondiabetic subjects and analyzed the potassium and glucose balance in the splanchnic bed and the periphery (19). This study is cited (20) to support concordant glucose and potassium uptake by cells because of the positive correlation of the fall in plasma [K ϩ ] (which is a composite of splanchnic and peripheral potassium transport) with glucose utilization. Note that the DeFronzo study separately examined splanchnic and peripheral potassium handling, which are both very complex; in fact, the authors concluded that there was no evidence in either system that potassium uptake is coupled to glucose uptake (19).…”

Section: Discussionmentioning

confidence: 99%

“…Hyperinsulinemic euglycemic clamps performed on 20 adolescents with insulin-dependent diabetes and 10 age-matched controls disclosed a slightly lower insulin-induced fall in plasma [K ϩ ] in diabetic subjects and a correlation between glucose disposal rate and fall in serum [K ϩ ] in control but not in diabetic subjects (20). It is unclear why this relationship is not maintained in diabetics if cell entry of glucose and potassium are coupled.…”

Section: Discussionmentioning

confidence: 99%

“…DeFronzo et al observed a relationship between the decline in plasma [K ϩ ] and insulin level as well the total amount of glucose taken up by cells (19). Arslanian et al concluded that insulin-dependent diabetics have impaired potassium uptake (20). However, Cohen et al found independent actions of insulin on glucose and potassium uptake (21).…”

Section: Introductionmentioning

confidence: 99%

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Comparison of Insulin Action on Glucose versus Potassium Uptake in Humans

Nguyen¹,

Maalouf²,

Sakhaee³

et al. 2011

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives Insulin has several physiologic actions that include stimulation of cellular glucose and potassium uptake. The ability of insulin to induce glucose uptake by cells is impaired in type 2 diabetes mellitus, but whether potassium uptake is similarly impaired is not known. This study examines whether the cellular uptake of these molecules is regulated in concert or independently.Design, setting, participants, & measurements Thirty-two nondiabetic and 13 type 2 diabetic subjects with normal GFR were given a similar, constant metabolic diet for 8 days. On day 9, they were subjected to a hyperinsulinemic euglycemic clamp for 2 hours. Serum and urinary chemistry were obtained before and during the clamp. Glucose disposal rate was calculated from glucose infusion rate during hyperinsulinemic euglycemia. Intracellular potassium and phosphate uptake were calculated by the reduction of extracellular potassium or phosphate content corrected for urinary excretion.Results Although glucose disposal rate tended to be lower in type 2 diabetics, cellular potassium uptake was similar between diabetics and nondiabetics. Additionally, although glucose disposal rate was lower with increasing body mass index (R 2 ϭ 0.362), cellular potassium (R 2 ϭ 0.052), and phosphate (R 2 ϭ 0.002), uptake rates did not correlate with body mass index. There was also no correlation between glucose disposal rate and potassium (R 2 ϭ 0.016) or phosphate uptake (R 2 ϭ 0.053).Conclusions Insulin-stimulated intracellular uptake of glucose and potassium are independent of each other. In type 2 diabetes, potassium uptake is preserved despite impaired glucose disposal.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Comparison of Insulin Action on Glucose versus Potassium Uptake in Humans

Nguyen¹,

Maalouf²,

Sakhaee³

et al. 2011

Clinical Journal of the American Society of Nephrology

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“…The resulting hyperinsulinemic may provoke hypokalemia secondary to stimulating excessive cellular K + uptake unless insulin’s action on K + uptake is similarly dampened. Impaired insulin action on K + fluxes has, indeed, been reported in obesity and diabetes (79, 80), which are both associated with insulin resistance with respect to glucose metabolism. However, insulin-mediated K + uptake is not altered in uremia, whereas insulin-mediated glucose uptake is markedly impaired (81).…”

Section: Molecular Mechanisms Of Extrarenal K+ Adaptationmentioning

confidence: 91%

Recent Advances in Understanding Integrative Control of Potassium Homeostasis

Youn

McDonough

2009

Annu. Rev. Physiol.

116

108

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The potassium homeostatic system is very tightly regulated. Recent studies have shed light on the sensing and molecular mechanisms responsible for this tight control. In addition to classic feedback regulation mediated by a rise in extracellular fluid (ECF) [K+], there is evidence for a feedforward mechanism: Dietary K+ intake is sensed in the gut, and an unidentified gut factor is activated to stimulate renal K+ excretion. This pathway may explain renal and extrarenal responses to altered K+ intake that occur independently of changes in ECF [K+]. Mechanisms for conserving ECF K+ during fasting or K+ deprivation have been described: Kidney NADPH oxidase activation initiates a cascade that provokes the retraction of K+ channels from the cell membrane, and muscle becomes resistant to insulin stimulation of cellular K+ uptake. How these mechanisms are triggered by K+ deprivation remains unclear. Cellular AMP kinase–dependent protein kinase activity provokes the acute transfer of K+ from the ECF to the ICF, which may be important in exercise or ischemia. These recent advances may shed light on the beneficial effects of a high-K+ diet for the cardiovascular system.

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“…On the other hand, Alvestrand et al (31) showed that insulin-mediated K ϩ uptake was not altered in uremia, whereas insulin-mediated glucose uptake was markedly impaired. Thus there is evidence for an association (29,30) as well as a dissociation (12,31) of resistance to insulin action on glucose versus K ϩ regulation. In those studies, however, insulin action on K ϩ fluxes in vivo was studied mainly by observing decreases in plasma K ϩ levels or measuring K ϩ uptake by specific organs (e.g., liver) during insulin infusion (29 -32).…”

Section: Insulin Actions On Glucose and Kmentioning

confidence: 99%

Independent Regulation of In Vivo Insulin Action on Glucose Versus K+ Uptake by Dietary Fat and K+ Content

et al. 2002

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Insulin stimulates both glucose and K؉ uptake, and high-fat feeding is known to decrease insulin-stimulated glucose uptake. The purpose of this study was to examine whether insulin's actions on glucose and K ؉ uptake are similarly decreased by a high-fat diet. Wistar rats were fed a standard control (12.2% fat; n ‫؍‬ 6) or high-fat (66.5% fat; n ‫؍‬ 13) diet for 15 days. Because K ؉ content was 1% in the control and 0.5% in the high-fat diet and because the rats ate less of the high-fat diet, we also compared the high-fat diet with 0.5% K ؉ (HFD; n ‫؍‬ 7) to a high-fat diet supplemented with 1.5% K

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Impaired insulin mediated potassium uptake in adolescents with IDDM

Cited by 9 publications

References 27 publications

Comparison of Insulin Action on Glucose versus Potassium Uptake in Humans

Comparison of Insulin Action on Glucose versus Potassium Uptake in Humans

Recent Advances in Understanding Integrative Control of Potassium Homeostasis

Independent Regulation of In Vivo Insulin Action on Glucose Versus K+ Uptake by Dietary Fat and K+ Content

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