Disorders of Carbohydrate and Lipid Metabolism in Uremia

Bagdade, John D.

doi:10.1159/000180445

Cited by 39 publications

(21 citation statements)

References 18 publications

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“…In contrast to these studies, Cattram et al (35) (Figs. 1 and 2); therefore, hyperlipidemia in uremia is solely due to defect(s) in clearance as previously suggested (1)(2)(3)(4)(5)(33)(34)(35).…”

Section: Discussionmentioning

confidence: 56%

“…Increased lipid production, reduced peripheral tissue removal, or a combination of both could contribute to hyperlipidemia in uremia (1,2). It is presently well established that abnormalities of lipoprotein lipase, the tissue enzyme system that mediates triglyceride removal, exist in uremia (3)(4)(5).…”

Section: Discussionmentioning

confidence: 99%

“…The precise mechanism(s) causing hypertriglyceridemia in renal failure remains unknown (1,2). It could be due to either increased triglyceride production by liver and/or reduced peripheral removal.…”

Section: Introductionmentioning

confidence: 99%

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Insulin resistance in uremia. Characterization of lipid metabolism in freshly isolated and primary cultures of hepatocytes from chronic uremic rats.

F¹,

Lanza-Jacoby²

1983

J. Clin. Invest.

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A B S T R A C T We have studied the mechanism(s) of hyperlipidemia and liver insulin sensitivity in a rat model of severe chronic uremia (U).Basal lipid synthesis was decreased in freshly isolated hepatocytes from U when compared with shamoperated ad lib.-fed controls (alfC). Basal lipid synthesis in pair-fed controls (pfC) was in between U and alfC. Similarly, the activity of liver acetyl CoA carboxylase, fatty acid synthetase, citrate cleavage enzyme, malate dehydrogenase, and glucose-6-phosphate dehydrogenase was diminished in U. Muscle and adipose tissue lipoprotein lipase was also decreased.Insulin stimulated lipid synthesis in freshly isolated hepatocytes from alfC. Hepatocytes from U and pfC were resistant to this effect of insulin. To ascertain if the insulin resistance in U was due to starvation (chow intake 50% of alfC) or to uremia itself, the U and pfC were intragastrically fed an isocaloric diet via a Holter pump the last week of the experimental period. Hepatocytes from orally fed U and pfC were also cultured for 24 h in serum-free medium. While freshly isolated and cultured U hepatocytes remained insulin resistant, those from pfC normalized, in vivo and in vitro, when they were provided with enough nutrients.Conclusions

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Section: Discussionmentioning

confidence: 56%

Section: Discussionmentioning

confidence: 99%

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Insulin resistance in uremia. Characterization of lipid metabolism in freshly isolated and primary cultures of hepatocytes from chronic uremic rats.

F¹,

Lanza-Jacoby²

1983

J. Clin. Invest.

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“…Calcitriol mainly influences the first phase of insulin release and its effect may be due to a direct action on the pancreatic [3-cell. The presence o f glucose metabolism abnormalities in uremic patients has long been recognized [1][2][3]. Both insulin resistance and reduced glucose sensitivity of pancreatic p-cells are the main causes [4][5][6][7][8][9].…”

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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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“…Chronic uraemia in the human is characterized by a number of metabolic abnormalities, including carbohydrate intolerance (Hampers et al, 1970;DeFronzo et al, 1973;Bagdade, 1975;DeFronzo & Alverstrande, 1980), insulin resistance (Westervelt, 1969;Roth et al, 1973), raised plasma glucagon (Bilbrey et al, 1974;Sherwin et al, 1976) and hypertriglyceridaemia (Bagdade, 1968(Bagdade, , 1970Bierman, 1970 Anderson & Bergstr6m, 1971;Brown et al, 1973;Lindholm et al, 1979;Grodstein et al, 1981), and this excessive absorption of carbohydrate may contribute to the hypertriglyceridaemia and obesity in some patients on long-term continuous ambulatory peritoneal dialysis (Nolph & Prowant, 1979;DeSanto et al, 1979).…”

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confidence: 99%

Effects of glucose-containing peritoneal-dialysis solutions on rates of lipogenesis in vivo in the liver, brown and white adipose tissue of chronic uraemic rats

Klim¹,

Williamson²

1983

Biochemical Journal

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1. Chronic uraemic rats had decreased food intake, and this was accompanied by decreased weight of the epididymal fat-pads and interscapular brown adipose tissue. Normal rats whose food intake was restricted to an amount similar to that of the uraemic rats showed similar decreases in weight of the adipose-tissue depots. In addition, the food-restricted rats had decreased liver weight compared with normal or uraemic rats. 2. The basal rate of lipogenesis was decreased in liver and epididymal fat-pads of food-restricted and uraemic rats and in interscapular brown adipose tissue of uraemic rats. 3. Administration of a low-glucose-containing (1.36%) peritoneal-dialysis solution slightly increased lipogenesis in liver of uraemic rats, but had no significant effect in epididymal fat-pads. For brown fat, the rate of lipogenesis was increased in normal, food-restricted and uraemic groups, but the values for the last group were 4-5-fold lower than for the food-restricted or control groups. 4. A high-glucosecontaining (3.86%) peritoneal-dialysis solution gave similar rates of lipogenesis in liver, epididymal fat-pads and brown fat of all three groups, but for brown fat moderately uraemic rats showed a considerably lower rate of lipogenesis than did mildly uraemic rats. 5. The basal plasma insulin concentration was lower in the food-restricted (50%) and uraemic (70%) groups than in the control group. The low-glucose peritonealdialysis solution increased plasma insulin to control values in the food-restricted rats, but had no significant effect on plasma insulin in the uraemic rats, despite a significant increase in blood glucose in this group. 6. It is concluded that there is an impairment of the lipogenic response to intraperitoneal glucose loads in interscapular brown adipose tissue of uraemic rats, and that this is not due to the accompanying decrease in food intake. The hypoinsulinaemia may be an important factor. The possible relevance of this finding to the obesity observed in some uraemic patients treated by peritoneal dialysis with glucose-containing solutions is discussed.

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Disorders of Carbohydrate and Lipid Metabolism in Uremia

Cited by 39 publications

References 18 publications

Insulin resistance in uremia. Characterization of lipid metabolism in freshly isolated and primary cultures of hepatocytes from chronic uremic rats.

Insulin resistance in uremia. Characterization of lipid metabolism in freshly isolated and primary cultures of hepatocytes from chronic uremic rats.

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

Effects of glucose-containing peritoneal-dialysis solutions on rates of lipogenesis in vivo in the liver, brown and white adipose tissue of chronic uraemic rats

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