Hyperzincuria in insulin treated diabetes mellitus—its relation to glucose homeostasis and insulin administration

McNair, Peter; Kiilerich, S.; Christiansen, C.; Christensen, Merete Sanvig; Madsbad, Sten; Transbøl, Ib

doi:10.1016/0009-8981(81)90457-5

Cited by 76 publications

(49 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We know that zinc-deficient animals have a lack of insulin in beta cells [3]. Alterations in zinc homeostasis appear to be related to diabetes: hyperzincuria seems well documented in both type 1 and type 2 diabetes and may be influenced by both sex and glycaemic status [4,5]. Plasma zinc may be low (type 2 diabetes) or high (type 1 diabetes) [6].…”

Section: Zinc and Diabetesmentioning

confidence: 99%

Zinc, zinc transporters and diabetes

Rungby

2010

Diabetologia

View full text Add to dashboard Cite

The role of zinc in islet function has recently achieved new attention as a consequence of the identification of zinc transporter 8 (ZNT8) in islets, and the association of mutations in the gene for this zinc transporter with glucose intolerance and type 2 diabetes. ZNT8 is also an autoantigen associated with the appearance of type 1 diabetes. A number of experimental models have been employed to suggest how ZNT8 and other zinc transporters regulate beta cell insulin processing and possibly secretion. An additional role for the zinc transporters in regulating alpha cell function has been suggested. In this issue of Diabetologia, Wijesekara and colleagues, using a cell-specific Znt8 (also known as Slc30a8) knockout model, demonstrate that beta cell insulin processing and glucose tolerance is negatively affected after beta cell knock out of Znt8, whereas Znt8 knockout in alpha cells seems to have little effect on glucagon secretion or glucose tolerance. Although we are yet to see the therapeutic potential of these new findings, the area represents a field through which manipulation of islet function may eventually be possible.

show abstract

Section: Zinc and Diabetesmentioning

confidence: 99%

Zinc, zinc transporters and diabetes

Rungby

2010

Diabetologia

View full text Add to dashboard Cite

show abstract

“…Zinc is known to be necessary for achieving better glycemic control and improvement in peripheral neuropathy as assessed by motor nerve conduction velocity (Hayee et al, 2005). Diabetics affects zinc metabolism in many ways McNair et al confirmed hyperzincuria in relationship to the degree of hyperglycaemia (McNair et al, 1981). Kinlaw et al demonstrated abnormal Zn tolerance test in diabetic patients suggestive of decreased absorption (Kinlaw et al, 1983).…”

Section: Resultsmentioning

confidence: 99%

Effect of Zinc Supplementation on Glycemic Control and Electrophysiological Recording (ESP. Brainstem Auditory Evoked Potential) in Diabetic Patients (NIDDM) with Neuropathy

Maheshwari¹,

Agrawal²,

Kumar³

et al. 2016

Int.J.Curr.Res.Aca.Rev

View full text Add to dashboard Cite

“…Other authors have suggested that changes in maternal levels of trace metals may be involved in t h e induction of congenital malformations both in humans (2,3,14,17,23) and animals (15,16). Diabetic individuals a r e furthermore known to lose t r a c e metals, via increased urinary output in relation to their degree of metabolic control (19). Altered levels of trace metals, in particular zinc, may therefore be of significance for the induction of malformations in diabetic pregnancy.…”

Section: Discussionmentioning

confidence: 99%

Induction of Skeletal Malformations in the Offspring of Rats Fed a Zinc Deficient Diet

Styrud

Dahlström

Eriksson

1986

Upsala Journal of Medical Sciences

View full text Add to dashboard Cite

Pregnant rats were subjected t o a t r a c e metal poor diet (1.2 ppm zinc, 5.9 ppm copper, 40 ppm manganese) during t h e entire gestation. The r a t mothers did not gain weight during pregnancy and showed decreased liver weight and lowered serum glucose levels on gestational day 20. The offspring exhibited decreased body and placental weights, delayed ossification of t h e skeleton, and a n increased resorption rate. We also found 4 % skeletal malformations in the offspring (0 % in t h e controls), which closely resembled a type of malformation previously encountered in rats when the mother was manifest diabetic (i..~. sacral dysgenesis). The zinc levels were decreased and manganese levels increased t o the same extent in offspring of trace metal restricted (this study) and manifest diabetic r a t s (previous studies). Furthermore, when pregnant rats on the trace metal restricted diet were resupplemented with 75 ppm zinc in t h e drinking water the offspring largely normalized their somatic and placental growth, skeletal maturation, as well as their zinc and manganese levels. In addition, the fetuses of the zinc resupplemented rats did not show any malformations. The possibility of common teratological mechanisms in maternal diabetes and t r a c e metal deficiency may therefore be considered.

show abstract

Hyperzincuria in insulin treated diabetes mellitus—its relation to glucose homeostasis and insulin administration

Cited by 76 publications

References 14 publications

Zinc, zinc transporters and diabetes

Zinc, zinc transporters and diabetes

Effect of Zinc Supplementation on Glycemic Control and Electrophysiological Recording (ESP. Brainstem Auditory Evoked Potential) in Diabetic Patients (NIDDM) with Neuropathy

Induction of Skeletal Malformations in the Offspring of Rats Fed a Zinc Deficient Diet

Contact Info

Product

Resources

About