The reduced secretion of, and sensitivity to insulin in zinc-deficient rats

Quarterman, J.; Mills, Christopher; Humphries, W. R.

doi:10.1016/0006-291x(66)90785-6

Cited by 122 publications

(45 citation statements)

References 8 publications

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“…Further studies are necessary to determine whether an enhancement of this process necessarily implies that transfer of glucose into the blood is accelerated in vivo. This is a matter of some importance as several reports have described reduced glucose tolerance in Zn-deficient rats given glucose by intraperitoneal injection, but not when the dose was given orally (Quarterman et al 1966;Hendricks & Mahoney, 1972). Another aspect of abnormal glucose metabolism in Zn-deficient rats has been described recently by Reeves & O'Dell(l983) who have shown a reduced incorporation of glucose from an oral dose into fatty acids, but increased…”

Section: Discussionmentioning

confidence: 96%

Hexose transport and mucosal morphology in the small intestine of the zinc-deficient rat

Southon¹,

Gee²,

Johnson³

1984

Br J Nutr

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1. Immature male Wistar rats were given a zinc-depleted semi-synthetic diet (2 mg Zn/kg diet) for 4 weeks.Control groups received a similar diet containing 60 mg Zn/kg diet, either ad lib. or in amounts matched to the consumption of the Zn-deficient group. Rates of growth and food conversion efficiency were markedly lower in the Zn-deficient group compared to controls.2. The phloridzin-sensitive uptake of galactose and 3-0-methyl glucose by everted jejunal rings from each group was measured over a range of concentrations. Kinetic analysis revealed that the maximum transport rate (Vmax) for the uptake of both sugars was significantly higher in the Zn-deficient group than in the control groups.3. The villi, microdissected from samples of proximal jejunum, were significantly shorter and narrower across the base in the Zn-deficient group than those of the control groups, but were present in greater numbers per unit serosal area.

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Section: Discussionmentioning

confidence: 96%

Hexose transport and mucosal morphology in the small intestine of the zinc-deficient rat

Southon¹,

Gee²,

Johnson³

1984

Br J Nutr

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“…Forty years ago, Quarterman et al demonstrated that zincdeprived rats had an impaired insulin secretion response to glucose stimulation (Quarterman et al, 1966), and other studies indicated decreased islet cell insulin content in zincdeficient states (Engelbart and Kief, 1970). In this study, total insulin was not significantly increased in ZnT-8-expressing cells despite higher zinc content, nor was insulin secretion in basal glucose conditions.…”

Section: Discussionmentioning

confidence: 99%

In vivo expression and functional characterization of the zinc transporter ZnT8 in glucose-induced insulin secretion

Chimienti

Devergnas

Pattou

et al. 2006

Journal of Cell Science

323

267

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Insulin-secreting pancreatic beta cells are exceptionally rich in zinc. In these cells, zinc is required for zinc-insulin crystallization within secretory vesicles. Secreted zinc has also been proposed to be a paracrine and autocrine modulator of glucagon and insulin secretion in pancreatic alpha and beta cells, respectively. However, little is known about the molecular mechanisms underlying zinc accumulation in insulin-containing vesicles. We previously identified a pancreas-specific zinc transporter, ZnT-8, which colocalized with insulin in cultured beta cells. In this paper we studied its localization in human pancreatic islet cells, and its effect on cellular zinc content and insulin secretion. In human pancreatic islet cells, ZnT-8 was exclusively expressed in insulin-producing beta cells, and colocalized with insulin in these cells. ZnT-8 overexpression stimulated zinc accumulation and increased total intracellular zinc in insulin-secreting INS-1E cells. Furthermore, ZnT-8-overexpressing cells display enhanced glucose-stimulated insulin secretion compared with control cells, only for a high glucose challenge, i.e. >10 mM glucose. Altogether, these data strongly suggest that the zinc transporter ZnT-8 is a key protein for both zinc accumulation and regulation of insulin secretion in pancreatic beta cells.

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“…The predominant effect of diabetes on zinc homeostasis is hypozincemia, which may result from hyperzincuria, decreased absorption, or both. Forty years ago, Quarterman et al (35) demonstrated that zinc-deprived rats had an impaired response of insulin secretion to glucose stimulation, and other studies (36) indicated a decreased islet cell insulin content in zincdeficiency states. Conversely, zinc supplementation markedly ameliorated the hyperglycemia of diabetic mice (37).…”

Section: Discussionmentioning

confidence: 99%

Identification and Cloning of a β-Cell–Specific Zinc Transporter, ZnT-8, Localized Into Insulin Secretory Granules

Chimienti¹,

Devergnas²,

Favier³

et al. 2004

Diabetes

440

340

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The reduced secretion of, and sensitivity to insulin in zinc-deficient rats

Cited by 122 publications

References 8 publications

Hexose transport and mucosal morphology in the small intestine of the zinc-deficient rat

Hexose transport and mucosal morphology in the small intestine of the zinc-deficient rat

In vivo expression and functional characterization of the zinc transporter ZnT8 in glucose-induced insulin secretion

Identification and Cloning of a β-Cell–Specific Zinc Transporter, ZnT-8, Localized Into Insulin Secretory Granules

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