Zinc’s role in the glycemic control of patients with type 2 diabetes: a systematic review

Carvalho, Gabrielli Barbosa de; Brandão-Lima, Paula Nascimento; Maia, Carla Soraya Costa; Barbosa, Kiriaque Barra Ferreira; Pires, Liliane Viana

doi:10.1007/s10534-017-9996-y

Cited by 51 publications

(33 citation statements)

References 51 publications

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“…After a stimulus for insulin release, amylin and zinc may be immediately co-distributed locally, but to date no evidence for interaction within the β- granule has emerged. In fact, zinc plays a role in glycemic control [61] and our results suggests that dietary zinc restriction induces a relative insulin resistance ( Fig. 1E ) and impaired endocrine pancreatic function associated with preferable apoptotic pattern despite the insulin crystallinity reached under moderate dietary zinc restriction ( Fig.…”

Section: Discussionmentioning

confidence: 84%

Zinc restriction promotes β-cell hyper-hormonemia and endocrine pancreas degeneration in mice

Sisnande

Lima

Silva

et al. 2019

Preprint

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Zinc is a key component of proteins, including interaction with varying pancreatic hormones, including insulin and amylin. Zinc is key in insulin crystallinity in ZnT8 knock-out mice models, although the dietary role of zinc restriction over both energetic metabolism and ß-pancreatic hormonemia and morphology remained unexplored. We aimed to test whether dietary zinc restriction on swiss male mice would impact over endocrine pancreas and metabolic phenotype. We evaluated the role of dietary zinc restriction on ß-pancreatic hormonemia on non-transgenic Swiss male mice weaned onto a control or low-zinc diet for 4 weeks. Growth, glycemia, insulinemia, amylinemia and pancreatic islet were smaller in intervention group despite insulin crystallinity in secretory granules. We have found overlabelling for insulin, amylin and toxic oligomers in apoptotic pancreatic islet. High production of β-pancreatic hormones in zinc-restricted animals counteract the decreasing islet size due to their apoptotic cells. We conclude that zinc deficiency is sufficient to promote islet β-cell hormonal disruption and degeneration.

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Section: Discussionmentioning

confidence: 84%

Zinc restriction promotes β-cell hyper-hormonemia and endocrine pancreas degeneration in mice

Sisnande

Lima

Silva

et al. 2019

Preprint

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“…They found that zinc supplementation improved liver conditions in type 2 Dm rat models through multiple pathways, in which GRP78 linked ER stress and LC3-II-linked autophagy are ameliorated to some degree. The results of a systematic review by Barbosa de Carvalho et al [60] about the role of zinc in patients with type 2 Dm confirming the role of zinc in controlling circulating glucose concentration through maintenance of insulin homeostasis. Based on these positive findings, the authors concluded that adequate dietetic ingestion and/or zinc supplementation are essential in the control of type 2 Dm.…”

Section: Main Textmentioning

confidence: 84%

Non-Alcoholic Fatty Liver Disease, Diabetes Mellitus, and Zinc/ Zinc Transporters: Is there a Connection?

Grüngreiff¹

2018

Liver Research and Clinical Management

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Immune response and metabolic regulation are closely connected with each other in such a way that dysfunction could lead to a variety of metabolic diseases such as obesity, diabetes mellitus (Dm), lipid metabolism disorders, and fatty liver disorders. Combined with uncritical "sugar-based" overeating and malnutrition, these multisystem metabolic diseases expand into a global epidemic. There are correlations between a fatty liver disease and diabetic metabolism state. A fatty liver leads to insulin resistance and thus to the development of a type 2 Dm; insulin resistance in turn augments the fatty liver. Zinc is a trace element of fundamental importance for a variety of biological processes. The liver is the main organ of the zinc metabolism. Metallothionein and zinc transporters are the key regulators of cellular zinc homeostasis. Molecular studies support the assumption of a correlation between zinc and Dm. Zinc is essential for the synthesis, secretion, and storage of insulin. ZnT8 is a significant autoantigen for type 1 Dm. Genetic polymorphisms in the ZnT8 gene are associated with an increased risk of developing type 2 Dm. Cellular zinc restriction induces the release of stress, particularly in the endoplasmic reticulum (ER). ER stress alone or coupled with cellular stress, as well as chronic inflammation, are central to the development of insulin resistance and type 2 Dm. The present insights into the context of a non-alcoholic fatty liver disease (NAFLD) and a type 2 Dm indicate that zinc and zinc transporters at the cellular level in various forms and in interactions with other mediators both in the regulation of physiological processes and in the formation of pathological processes, such as the cellular and ER stress, as well as chronic inflammation, and the development of metabolic disorders are involved.

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“…An earlier systematical evaluation of the literature and meta-analysis of the effects of zinc supplementation on diabetes reported that zinc supplementation has beneficial effects on glycemic control and promotes healthy lipid parameters [15]. This was further confirmed by subsequent systemic review, showed that zinc supplementation in T2D patients has improved glycemic control, since the %HbA1c significantly reduced in these individuals [16]. In addition, a recent randomized, doubleblind, placebo-controlled trial confirmed that zinc supplementation for 12 weeks among diabetic foot ulcer patients had beneficial effects on parameters of ulcer size and metabolic profiles [17].…”

Section: Introductionmentioning

confidence: 84%

Preventing Diabetes and Diabetic Cardiovascular Diseases with Dietary Zinc

Cai¹

2017

J Microb Biochem Technol

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Zinc’s role in the glycemic control of patients with type 2 diabetes: a systematic review

Cited by 51 publications

References 51 publications

Zinc restriction promotes β-cell hyper-hormonemia and endocrine pancreas degeneration in mice

Zinc restriction promotes β-cell hyper-hormonemia and endocrine pancreas degeneration in mice

Non-Alcoholic Fatty Liver Disease, Diabetes Mellitus, and Zinc/ Zinc Transporters: Is there a Connection?

Preventing Diabetes and Diabetic Cardiovascular Diseases with Dietary Zinc

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