The Effect of Dialysis on the Carbohydrate Intolerance of Chronic Renal Failure

Spitz, I; Ah, Rubenstein; Bersohn, I; Am, Lawrence; Kirsteins, L.

doi:10.1055/s-0028-1095114

Cited by 20 publications

(9 citation statements)

References 15 publications

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“…The The importance of altered tissue responsiveness to ision of gluca-glucagon in uremia is underscored by the differential infusion rate in effects of dialysis on glucose tolerance and plasma glune response in e consequently cagon levels. Although, in according with previous mbined in the reports (5,(9)(10)(11)(12), dialysis was associated with an imf the changes provement in glucose tolerance (Fig. 4), plasma glu-L1 subjects (at cagon levels remained unchanged.…”

Section: Discussionsupporting

confidence: 75%

“…Decreased sensitivity to the hypoglycemic effects of endogenous (2,5,6) and exogenous (3,(5)(6)(7)(8) insulin has been observed in uremic man, whereas basal and glucose-stimulated insulin concentrations are normal or increased (1-3, 5, 6, 9). After chronic dialysis, glucose tolerance generally improves in association with increased tissue sensitivity to insulin (5,(9)(10)(11)(12)(13). The mechanism of uremia-induced insulin resistance and the improvement in insulin sensitivity after dialysis has not been established.…”

Section: Introductionmentioning

confidence: 99%

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Influence of uremia and hemodialysis on the turnover and metabolic effects of glucagon.

Sherwin¹,

Bastl²,

Finkelstein³

et al. 1976

J. Clin. Invest.

196

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A B S T R A C T To evaluate the mechanism and role of hyperglucagonemia in the carbohydrate intolerance of uremia, 19 patients with chronic renal failure (12 of whom had undergone chronic hemodialysis for at least 11 mo) and 35 healthy control subjects were studied. Plasma glucagon, glucose, and insulin were measured in the basal state, after glucose ingestion (100 g), after intravenous alanine (0.15 g/kg), and during a 3-h continuous infusion of glucagon (3 ng/kg per min) which in normal subjects, raised plasma glucagon levels into the upper physiological range.Basal concentrations of plasma glucagon, the increment in glucagon after infusion of alanine, and postglucose glucagon levels were three-to fourfold greater in uremic patients than in controls. The plasma glucagon increments after the infusion of exogenous glucagon were also two-to threefold greater in the uremics. The metabolic clearance rate (MCR) of glucagon in uremics was reduced by 58% as compared to controls. In contrast, the basal systemic delivery rate (BSDR) of glucagon in uremics was not significantly different from controls.Comparison of dialyzed and undialyzed uremics showed no differences with respect to plasma concentrations, MCR, or BSDR of glucagon. However, during the infusion of glucagon, the increments in plasma glucose in undialyzed uremics were three-to fourfold greater than in dialyzed uremics or controls. When the glucagon infusion rate was increased in controls to 6 ng/kg per min to produce increments in plasma glucagon comparable to uremics, the glycemic response remained approximately twofold greater in the undialyzed uremics. The plasma glucose response to glu- cagon in the uremics showed a direct linear correlation with oral glucose tolerance which was also improved with dialysis. The glucagon infusion resulted in a 24% reduction in plasma alanine in uremics but had no effect on alanine levels in controls. It is concluded that (a) hyperglucagonemia in uremia is primarily a result of decreased catabolism rather than hypersecretion of this hormone; (b) sensitivity to the hyperglycemic effect of physiological increments in glucagon is increased in undialyzed uremic patients; and (c) dialysis normalizes the glycemic response to glucagon, possibly accounting thereby for improved glucose tolerance despite persistent hyperglucagonemia. These findings thus provide evidence of decreased hormonal catabolism contributing to a hyperglucagonemic state, and of altered tissue sensitivity contributing to the pathophysiological action of this hormone.

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Section: Discussionsupporting

confidence: 75%

Section: Introductionmentioning

confidence: 99%

Influence of uremia and hemodialysis on the turnover and metabolic effects of glucagon.

Sherwin¹,

Bastl²,

Finkelstein³

et al. 1976

J. Clin. Invest.

196

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“…Suppression of plasma GH concentrations in normal individuals with intravenous glucose infusion is well documented (24). In approximately 60% of patients with CRF, fasting GH is abnormally elevated and, paradoxically, rises during glucose infusion (25)(26)(27). Our studies reconfirm this observation.…”

Section: Introductionsupporting

confidence: 81%

Hyperglucagonemia of Renal Failure

Bilbrey¹,

Faloona²,

White³

et al. 1974

J. Clin. Invest.

159

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“…Both insulin resistance and reduced glucose sensitivity of pancreatic p-cells are the main causes [4][5][6][7][8][9]. Resistance to the hypo glycemic action o f insulin in the peripheral tissues is univer sal among uremic patients [4][5][6][7][8][9], Insulin response to hyper glycemia has been reported to be normal [10], increased [11] or decreased [1] when evaluated in absolute terms but it is lower than in controls if compared to the magnitude of pancreatic (1-cell glicidic stimulation [4,9] or to insulin resistance degree [7]. The mechanisms responsible for this inhibition o f insulin secretion are still unclear.…”

mentioning

confidence: 99%

Glucose-Induced Insulin Secretion in Uremia: Role of 1α,25(HO)<sub>2</sub>-Vitamin D<sub>3</sub>

Allegra¹,

Luisetto²,

Mengozzi³

et al. 1994

Nephron

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To evaluate the role and mechanism of action of calcitriol on glucose-induced insulin secretion in uremia, 17 patients with severe chronic renal failure were studied. Glucose metabolism was investigated by the intravenous glucose tolerance test (IVGTT) before and after treatment for 21 days with 0.5 µg/day of calcitriol and 500 mg/day of calcium (C + Ca) (6 cases) or 0.5 µg/day of calcitriol alone (C) (11 cases). After these evaluations the patients on C + Ca were shifted to C and 6 patients on C were shifted to C + Ca, and IVGTT was repeated 21 days after the shift. For each test plasma glucose (G), immunoreactive insulin (IRI) and C-peptide (C-p) were measured at -30,0,2,5,15,30,45,60 min, and baseline plasma values of 1α,25(HO)₂-vitamin D₃, C-terminal parathyroid hormone (PTH-C), intact parathyroid hormone (PTH-I), calcitonin, and serum values of total and ionized calcium were dosed. Also, glucose constant decay (K-G), insulin response (IRI area), C-p production (C-p area), insulinogenic index (IGI) and insulin resistance index (RI) were calculated. A historical group of 21 healthy volunteers formed the normal controls. 1α,25(HO)₂-vitamin D₃ plasma levels in uremic patients before treatment were significantly lower than normal range. As compared to controls, uremic patients showed significantly lower K-G, IRI area and IGI values and significantly higher RI values. After treatment with C or C + Ca, the insulin response improved significantly at 2 and 5 min and G decrement was more marked at 30,45 and 60 min. K-G and 0-15 min IRI area, 0-15 min IGI and 0-15 min C-p area values increased significantly but did not reach the normal values. Serum calcium and plasma 1α,25(HO)₂-vitamin D₃ levels significantly increased after treatment but no correlations were found between changes in glucose metabolism parameters and changes in total or ionized serum calcium or changes in 1α,25(HO)₂-vitamin D₃ plasma levels. Serum calcium values significantly decreased after shift from C + Ca to C and significantly increased after shift from C to C + Ca, but glucose metabolism parameters showed no further changes. From these data we inferred that 1α,25(HO)₂-vitamin D₃ deficiency may contribute to the inhibition of glucose-induced insulin secretion in uremia. Calcitriol mainly influences the first phase of insulin release and its effect may be due to a direct action on the pancreatic β-cell.

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The Effect of Dialysis on the Carbohydrate Intolerance of Chronic Renal Failure

Cited by 20 publications

References 15 publications

Influence of uremia and hemodialysis on the turnover and metabolic effects of glucagon.

Influence of uremia and hemodialysis on the turnover and metabolic effects of glucagon.

Hyperglucagonemia of Renal Failure

Glucose-Induced Insulin Secretion in Uremia: Role of 1α,25(HO)<sub>2</sub>-Vitamin D<sub>3</sub>

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