Glucose-6-Phosphate-Dehydrogenase Deficiency in Leprosy

Kher, Mrunal; Grover, Shobha

doi:10.1016/s0140-6736(69)92257-0

Cited by 11 publications

(4 citation statements)

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“…The fate of glucose through the PPP has not been well characterized and there is conflicting evidence about the activity of G6PD, the first/rate limiting enzyme in the PPP, in diabetes. For example, some studies suggest that G6PD activity is inhibited and NADPH is decreased in islets cells [26], Leydig cells [27], kidneys [28], lens [29], heart [30] and the liver [31] of type 1 diabetic rats (induced by streptozotocin- and alloxan-treatment); and in the liver [32], mononuclear leukocytes [33] and erythrocytes [34] of chronic diabetic patients. In contrast, recent studies have shown that G6PD is over-expressed in the adipocytes of obese (including db/db , ob/ob , and diet-induced obesity) mice, adipocytes and stromal-vascular cells of diabetic db/db mice, and adipocytes cultured, in vitro, under high glucose conditions [35, 36].…”

Section: Discussionmentioning

confidence: 99%

Synergistic activation of glucose-6-phosphate dehydrogenase and NAD(P)H oxidase by Src kinase elevates superoxide in type 2 diabetic, Zucker fa/fa, rat liver

Gupte

Floyd

Kozicky

et al. 2009

Free Radical Biology and Medicine

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Glucose metabolism through glycolysis and hexosamine pathway has been shown to be altered in type 2 diabetes. However, its fate through the pentose phosphate pathway (PPP) is currently unclear. In this study, we determined whether the activity of glucose-6-phosphate dehydrogenase (G6PD), the rate-limiting enzyme in the PPP, is modulated in the liver of Zucker obese fa/fa rats (9–11 weeks old). We found that G6PD expression and activity, NADPH levels and 6-phosphogluconate generation was significantly increased in liver of fa/fa rats. Inhibition of PI3 kinase and Src kinases decreased (P<0.05) G6PD activity in the fa/fa but not in the lean rat liver, suggesting that G6PD activity is regulated by PI3/Src kinase signaling pathways. G6PD-derived NADPH increased (P<0.05) superoxide anion levels by 70–90% in the fa/fa vs the lean rat liver, which was inhibited by NADPH oxidase inhibitor, gp91ds-tat (50 μM), and G6PD inhibitors, 6-aminonicotinamide (1 mM) and dihydroepiandrosterone (100 μM); therefore, indicating that elevated G6PD activity may be responsible for mediating superoxide generation. Interestingly, we also found a positive correlation between liver hypertrophy/increased G6PD activity (r2=0.77; P=0.0009) and liver hypertrophy/superoxide production (r2=0.51; P=0.0091) in fa/fa rats. Increased G6PD and NADPH oxidase expression and activity, in young hyper-glycemic and -insulinemic rats prior to the development of diabetes, appear to be contributing factors for the induction of oxidative stress. Since inhibition of G6PD activity decreases oxidative stress, we conclude that it behaves as a pro-oxidant in the fa/fa rat liver, in type 2 diabetes.

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Section: Discussionmentioning

confidence: 99%

Synergistic activation of glucose-6-phosphate dehydrogenase and NAD(P)H oxidase by Src kinase elevates superoxide in type 2 diabetic, Zucker fa/fa, rat liver

Gupte

Floyd

Kozicky

et al. 2009

Free Radical Biology and Medicine

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“…It has been reported that there is a higher incidence of G6PD deficiency among lepers (Kher and Grover, 1969). We thought it worthwhile to verify this in a Chinese population and also to study the incidence of abnormal haemoglobins in lepers compared to healthy subjects.…”

mentioning

confidence: 81%

Distribution of ABO blood groups, G6PD deficiency, and abnormal haemoglobins in leprosy.

Saha¹,

Wong²,

Banerjee³

et al. 1971

Journal of Medical Genetics

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“…6 They also commented that leprosy might be commoner in G6PD deficient cases, as a previous study had found that the prevalence of G6PD deficiency in the general population of the same area was just 9.6%. 7 However, they also found that there were no significant differences in incidences of the deficiency in different types of leprosy, thus concluding that the G6PD deficiency did not have an effect on the development of different types of leprosy.…”

Section: Discussionmentioning

confidence: 96%

Study on estimation of glucose-6-phosphate dehydrogenase in patients prior to initiation of dapsone therapy in leprosy

Agarwala

Sharma

2019

Int J Res Dermatol

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Background: Administration of dapsone in glucose-6-phosphate dehydrogenase (G6PD) deficient patients can lead to hemolysis which may be severe enough to warrant discontinuation of the drug. Screening for G6PD deficiency in leprosy patients before initiating treatment can prevent such adverse events. Methods: Medical records of all leprosy patients presenting between 1st January 2018 to 30th June 2018 were reviewed. G6PD levels, if done, were recorded for all patients needing dapsone therapy. Results: Of the 62 patients requiring treatment with dapsone (43 outpatients and 19 inpatients), G6PD estimation was done in 43 cases, i.e., 60.46% (26/43) of outpatients and 89.4% (17/19) of inpatients.10 patients were found deficient (6/26 outpatients and 4/17 inpatients). Conclusions: G6PD levels were not uniformly estimated in all patients requiring dapsone therapy. It was done more commonly estimated in inpatients (89.4%) when compared to outpatients (60.46%). The deficient G6PD levels were seen in 16% cases.

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Glucose-6-Phosphate-Dehydrogenase Deficiency in Leprosy

Cited by 11 publications

References 1 publication

Synergistic activation of glucose-6-phosphate dehydrogenase and NAD(P)H oxidase by Src kinase elevates superoxide in type 2 diabetic, Zucker fa/fa, rat liver

Synergistic activation of glucose-6-phosphate dehydrogenase and NAD(P)H oxidase by Src kinase elevates superoxide in type 2 diabetic, Zucker fa/fa, rat liver

Distribution of ABO blood groups, G6PD deficiency, and abnormal haemoglobins in leprosy.

Study on estimation of glucose-6-phosphate dehydrogenase in patients prior to initiation of dapsone therapy in leprosy

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