Diabetes mellitus and infection

Larkin, John G.; Frier, B. M.; Ireland, John

doi:10.1136/pgmj.61.713.233

Cited by 105 publications

(59 citation statements)

References 36 publications

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“…The incidence of a recognized group of rare infections is definitely high in diabetes mellitus or confined almost entirely to diabetic patients (Larkin et al 1985). Infectious diseases, particularly tuberculosis, were a major cause of death among diabetic patients before the advent of insulin therapy (Eliopoulos 1995).…”

Section: Introductionmentioning

confidence: 99%

Diabetes causes marked changes in lymphocyte metabolism

Otton

Mendonça²,

Curi³

2002

Journal of Endocrinology

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Section: Introductionmentioning

confidence: 99%

Diabetes causes marked changes in lymphocyte metabolism

Otton

Mendonça²,

Curi³

2002

Journal of Endocrinology

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“…The increased sensitivity to infections in diabetes [1,2] has long been associated with changes in neutrophil function [3][4][5]. However, while most studies have focused on the involvement of hyperglycemia in the defective neutrophil function, less effort has been made to investigate the role of insulin in normal function of neutrophil granulocytes.…”

Section: Introductionmentioning

confidence: 99%

Hyperglycemia in vitro attenuates insulin-stimulated chemokinesis in normal human neutrophils. Role of protein kinase C activation

Oldenborg

Sehlin

1999

Journal of Leukocyte Biology

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This study was performed to test whether the inhibitory effect of elevated D-glucose concentrations on insulin-stimulated chemokinesis in normal human neutrophils is mediated by increase in protein kinase C (PKC) activity. Activation of PKC with phorbol 12-myristate 13-acetate (PMA) at 0-100 nM dose-dependently inhibited neutrophil random locomotion in the absence of insulin. Suboptimal concentrations of PMA (0.1-0.5 nM) inhibited the chemokinetic effect of 160 U/mL insulin in a dose-dependent way. The specific PKC inhibitor bisindolylmaleimide (GF 109203x) did not affect the insulin-stimulated chemokinesis at 5 mM glucose but restored the chemokinetic effect of insulin at 15 mM glucose. These results therefore suggest that glucose-induced PKC activation may mediate the inhibitory effects of high glucose levels on insulin-stimulated chemokinesis in normal human neutrophils. J. Leukoc. Biol. 65: 635-640; 1999.

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“…Although varying among patients, long term complications of diabetes can also include changes in arteries (atherosclerosis), basement membranes of small vessels (microangiopathy), kidneys (nephropathy), retina (retinopathy), and nerves (neuropathy) (Vlassara et al 1984, Yabe-Nishimura 1998, Brownlee 2001 It has generally been stated that uncontrolled type 1 diabetic patients are more susceptible to bacterial and fungal infections than normal controls, though the cause has not yet been determined (Larkin et al 1985). In order to investigate this point, experimental models of diabetes have been developed from which chemical induction with alloxan has been the most widely used (Rerup 1970).…”

mentioning

confidence: 99%