Maternal zinc intake of Wistar rats has a protective effect in the alloxan-induced diabetic offspring

Abstract

Zinc has a role in the synthesis, storage, and secretion of insulin, and has been suggested to be beneficial when used in the diabetic state. Effect of zinc intake in pregnant rats has been studied here on diabetized offspring. Pregnant rats were divided in two groups; the control group received normal food and water, and the experimental group received zinc sulfate during pregnancy and 3 weeks after offspring birth. Male offspring from the control (C) and experimental (E) groups were divided each in three groups: C1, fed with normal food and water; C2, diabetized with alloxan; C3, received zinc sulfate; E1, fed with normal food and water; E2, diabetized with alloxan; and E3, receiving zinc sulfate. After 30 days, the histological changes of pancreatic tissues were investigated by light microscopy. Body weight, blood glucose, serum insulin levels, food intake, water intake, and urine quantity were also compared between the groups. Water intake and urine quantity were decreased significantly (p < 0.01 and p < 0.001) in E2 (experimental diabetic group) in comparison with C2 (control diabetic group), but there was no significant difference in the body weight in C2 in comparison with E2, while blood glucose was decreased significantly (p < 0.001) and blood insulin level was increased significantly (p < 0.01) in E2 in comparison with C2. Microscopic evaluation of pancreas showed that E2 were protected against alloxan-induced beta-cell degeneration. In conclusion, this work showed that maternal zinc intake may influence subsequent deleterious effects of diabetes on alloxan-diabetized offspring.

Low perinatal zinc status is not associated with the risk of type 1 diabetes in children

“…Rodent studies reported that zinc supplementation during pregnancy can protect the offspring against experimentally induced T1D . Zinc supplementation in the rodent model studies appeared to be supra‐physiological.…”

“…Oxidative stress is involved in the destruction of pancreatic β‐cells and the antioxidant properties of zinc may protect against T1D . Both population‐based and rodent studies report that zinc supplementation decreases the risk of T1D . A population‐based study reports, that zinc has an U‐shaped effect on the risk of T1D .…”

“…Moreover, maternal zinc deficiency may reduce the proliferation of β‐cell during fetal life . Rodent studies indicate that supplementation of zinc during pregnancy can lead to protection against T1D in the offspring …”

Differential Expression of Dicer, miRNAs, and Inflammatory Markers in Diabetic Ins2+/− Akita Hearts

“…Akita mice become diabetic spontaneously at the age of 3–4 weeks and show robust hyperglycemia by 12 weeks (2–7). Therefore, it is a better than the induced diabetes models such as NOD-autoimmune depletion of beta cells (8), OVE 26-the non-specific gene expression of beta cells (9), and Streptozotocin- or Alloxan-chemicals destruction of beta cells (10–12). These mice develop cardiac fibrosis, endothelium-myocyte uncoupling (5;13), impaired contractility of cardiomyocytes and cardiac dysfunction (4;14).…”

Zinc protection in fetal rats for maternal mercury exposure‐induced growth retardation is probably associated with S100B expression

“…For example, zinc itself may benefit the overall development of the pregnant rats and fetus as nutrition, resulting in the observed fetal development improvement. Maternal zinc intake has other benefits, such as protecting alloxan‐induced diabetic offspring and nickel‐induced hepatotoxicity . Furthermore, rats co‐administered with zinc displayed reduced mercury levels in the placenta, suggesting that the decreased mercury‐induced toxicity in fetuses might also be attributed to the ability of zinc to decrease the absorption of mercury into the maternal body.…”