Elsevier

Metabolism

Volume 37, Issue 2, February 1988, Pages 125-130
Metabolism

Impaired glucose handling in active rheumatoid arthritis: Relationship to peripheral insulin resistance

https://doi.org/10.1016/S0026-0495(98)90005-1Get rights and content

Abstract

Glucose metabolism was studied after an intravenous glucose loading in normal-weighted, previously untreated patients (n = 14) with active rheumatoid arthritis (RA). The patients displayed an enhanced insulin response and impaired glucose handling compared with healthy controls (P < .001). The insulin sensitivity, measured as the glucose utilization rate during steady state of euglycemia (M) was significantly decreased (P < .01) among the patients compared to the controls (5.5 ± 1.9 mg/kg BW/min [mean ± SD] and 7.2 ± 1.2, respectively). The corresponding values for the metabolic clearance rate (MCR) were 5.8 ± 0.6 mL/kg BW/min and 8.2 ± 0.4, respectively (P < .01). In the patient group the k value correlated with the peripheral insulin sensitivity (P < .01), which, in turn, was inversely related to the acute phase reaction (P < .05). During 1 week of potent anti-inflammatory treatment with corticosteroids (prednisolone 20 mg daily) the k value improved P < .001), the insulin sensitivity tended to improve and the insulin response increased (P < .001) after an intravenous glucose loading. Five patients who had a remission of their disease on sulphasalazine as antirheumatic therapy were reexamined. A normalization of the inflammatory activity as well as the glucose handling and insulin sensitivity was achieved. The data obtained indicate that impaired glucose handling in active RA is related to insulin resistance. The linkage between inflammatory indices and glucose metabolism might reflect a special consequence of inflammation, but the influence of nonspecific disease manifestations, ie, malnutrition, inactivity, and myopenia, has to be considered. Furthermore, measurements of plasma C-peptide concentrations and the calculation of the C-peptide to insulin molar ratio suggested that the hyperinsulinemia in active RA was partly due to an impaired hepatic extraction of insulin.

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    Supported by the Medical Faculty of the University of Uppsala and the Swedish Medical Research Council.

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