Uremia and Insulin Response

Westervelt, Frederic B.

doi:10.1001/archinte.1970.00310110135024

Cited by 20 publications

(9 citation statements)

References 2 publications

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“…These results suggest that the major site of insulini resistance in uremia resides in the periphery and are consistent with previous reports using the forearm infusion technique in chronically uremic man (27,28). Mondon et al (29) have reported similar results in rats made acutely uremic by bilateral nephrectomy.…”

Section: Discussionsupporting

confidence: 93%

Insulin resistance in uremia.

et al. 1981

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A B S T R A C T Tissue sensitivity to insulin was examined with the euglycemic insulin clamp technique in 17 chronically uremic and 36 control subjects. The plasma insulin concentration was raised by -100 ,uU/ ml and the plasma glucose concentration was maintained at the basal level with a variable glucose infusion. Under these steady-state conditions of euglycemia, the glucose infusion rate is a measure of the amount of glucose taken up by the entire body. In uremic subjects insulin-mediated glucose metabolism was reduced by 47% compared with controls (3.71 +0.20 vs. 7.38+0.26 mg/kg-min; P < 0.001). Basal hepatic glucose production (measured with [3H]-3-glucose) was normal in uremic subjects (2.17+0.04 mg/kg-min) and suppressed normally by 94±+2% following insulin administration. In six uremic and six control subjects, net splanchnic glucose balance was also measured directly by the hepatic venous catheterization technique. In the postabsorptive state splanchnic glucose production was similar in uremics (1.57+0.03 mg/kg.min) and controls (1.79+0.20 mg/ kg min). After 90 min of sustained hyperinsulinemia, splanchnic glucose balance reverted to a net uptake which was similar in uremics (0.42±0.11 mg/kg-min) and controls (0.53+0.12 mg/kg.min). In contrast, glucose uptake by the leg was reduced by 60% in the uremic group (21+1 vs. 52+8 ,umol/min kg of leg wt; P < 0.005) and this decrease closely paralleled the decrease in total glucose metabolism by the entire body. These results indicate that: (a) suppression of hepatic glucose production by physiologic hyperinsulinemia is not impaired by uremia, (b) insulinmediated glucose uptake by the liver is normal in uremic subjects, and (c) tissue insensitivity to insulin is the primary cause of insulin resistance in uremia.

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Section: Discussionsupporting

confidence: 93%

Insulin resistance in uremia.

et al. 1981

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“…Furthermore, glucagon ( (1). The reduction in glucose tolerance is characterized by increased insulin levels (2) and diminished responses to endogenous (3) and exogenous insulin (4), suggesting insulin resistance. In addition to alterations in insulin, uremia is characterized by hyperglucagonemia (5,6) and an increased sensitivity to glucagon-induced hyperglycemia (6).…”

mentioning

confidence: 99%

Glucagon and Insulin Binding to Liver Membranes in a Partially Nephrectomized Uremic Rat Model

Soman¹,

Felig²

1977

J. Clin. Invest.

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A B S T R A C T To investigate the role of glucagon and insulin receptor binding in the glucagon hypersensitivity and insulin resistance which characterize the glucose intolerance of uremia, liver plasma membranes were prepared from control rats (blood urea nitrogen [BUN] 15±1 mg/100 ml, creatinine 0.7±0.2 mg/100 ml), and from 70% nephrectomized rats (BUN 30±2 mg/100 ml, creatinine 2.2±0.2 mg/100 ml), and from 90% nephrectomized rats (BUN 46±3 mg/100 ml, creatinine 4.20+0.7 mg/100 ml), 4 wk after surgery. As compared to controls, the 90% nephrectomized rats had significantly higher levels of plasma glucose (95 ±4 vs. 125±11 mg/100 ml), plasma insulin (28±9 vs. 52±11 uU/ml), and plasma glucagon (28±5 vs. 215 ±18 pg/ml). Similar, but less marked, elevations were observed in the 70% nephrectomized animals.In liver plasma membranes from nephrectomized

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“…Decreased sensitivity of peripheral tissues to insulin seems well established. The results of forearm perfusion studies (1)(2)(3), the presence of elevated fasting immunoreactive insulin levels in uremia (4)(5)(6)(7)(8)(9), and the delayed and diminished glucose response after exogenous insulin (5,(9)(10)(11)(12)(13)(14)(15) and tolbutamide (4,9,11,(14)(15)(16) indicate the presence of insulin resistance in the majority of patients with chronic renal failure. In contrast, conflicting reports have appeared on the plasma insulin response to intravenous and oral glucose in uremia.…”

Section: Introductionmentioning

confidence: 99%

“…The continuous insulin infusion (40 mU/M2 surface area per min) was maintained for 70 min.3 All experiments were continued for an addi2Abbreviations used in this paper: I, plasma insulin level; M, glucose metabolism; MCR, metabolic clearance rate. 3 In patients 2, 9, and 10 the continuous infusion was extended to 120 min. tional 40 min after the infusion was stopped.…”

Section: Introductionmentioning

confidence: 99%