Glycated Haemoglobin Is Inversely Related to Serum Vitamin D Levels in Type 2 Diabetic Patients

Zoppini, Giacomo; Galletti, Anna Maria Raspolli; Targher, Giovanni; Brangani, Corinna; Pichiri, Isabella; Negri, Carlo; Stoico, Vincenzo; Cacciatori, V.; Bonora, Enzo

doi:10.1371/journal.pone.0082733

Cited by 54 publications

(45 citation statements)

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“…Glycated hemoglobin-an important indicator of the severity of diabetes-is reported to have an inverse relationship with circulating vitamin D levels [15]. The present study investigates the role of vitamin D supplementation using 2 vitamin D metabolites cholecalciferol and calcitriol in glycation prevention of HSA.…”

Section: Discussionmentioning

confidence: 99%

“…This can be reversed by supplementing vitamin D in diet in the form of cholecalciferol. But there is a rare possibility that low levels of circulating vitamin D may result from altered liver hydroxylase activity following onset of the diabetes as this enzyme catalyzes the first hydroxylation required for conversion of cholecalciferol to calcitriol [15]. Hence both, the functionally active forms of vitamin D, calcitriol, and the dietary vitamin D supplement, cholecalciferol, have been studied for their action on protein glycation in vitro.…”

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confidence: 99%

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Vitamin D prevents glycation of proteins: an in vitro study

2016

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Human serum albumin (HSA) is an important protein involved in the transport of hormones, fatty acids, drugs, and other macromolecules. Under hyperglycemic conditions, this molecule undergoes irreversible modification that affects its structure and function. In this study, we explored the effect of two forms of vitamin D, a nutraceutical, on glycation modification in HSA. The protein was incubated with a physiologically high concentration of glucose in the presence of vitamin D metabolites. After 21 days, samples were tested for secondary structural changes, side chain modification, and the presence of advanced glycation end products. Vitamin D metabolites could reduce glycation modification, albeit only to a small extent. Interaction studies reveal that Vitamin D interaction with HSA can prevent protein glycation.Keywords: calcitriol; glycation; protein Type 2 Diabetes is a global health issue growing at an unprecedented rate. The disease accounts for 90% of diabetes cases worldwide and is characterized by defects in glucose metabolism [1]. Persistently high blood glucose concentration encountered in diabetes often initiates Maillard reaction which causes nonenzymatic glycation of proteins and yields a plethora of reactive compounds called advanced glycation end products (AGEs) [2].Modification of protein structure and function by AGEs is consistent with the progression of diabetic complications and correlates positively with the severity of conditions like retinopathy, neuropathy, and nephropathy [3]. Once initiated, AGEs formation continues throughout the lifespan of proteins, and cannot be reversed by normalizing hyperglycemia [2,4].Human serum albumin (HSA) frequently undergoes Maillard reaction to from covalently cross-linked composites [3]. In normal adults, 6-10% of lysine chains are modified by nonenzymatic glycation, however, this number increases by 2-3 folds in individuals suffering from diabetes [5]. This may interfere with HSA function [5]. Since HSA is involved in the transportation of several moieties: nutrients, steroids, and a wide variety of drugs this can have detrimental physiological effects [6].Research suggests that vitamin D is involved in controlling AGE-associated damage in both diabetes and heart disorders [7]. Vitamin D is a fat-soluble micronutrient which is produced in the body by UV irradiation of a precursor steroid stored in the skin. The functionally active form of vitamin D, calcitriol, has a wide array of health implications [8]. Multiple studies have demonstrated its ability in limiting oxidative damage and regulating the status of a potent cellular antioxidant-reduced glutathione (GSH) [7]. Vitamin D deficiency is thought to be a risk factor for the development of diabetes; Low vitamin D status is associated with increased insulin resistance, glycated hemoglobin (HbA1c), and AGE formation [9][10][11]. Previous reports have correlated low circulating concentrations of vitamin D with increased risk of diabetic macrovascular and microvascular complications: mainly nephropathy a...

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Vitamin D prevents glycation of proteins: an in vitro study

2016

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“…Zoppini и соавт. в своем исследовании показали, что концен-трация циркулирующего в сыворотке больных СД2 активного метаболита витамина D обратно пропор-циональна уровню HbA 1c , что остается статистиче-ски достоверным после мультивариантного анализа с учетом возраста, ИМТ, продолжительности забо-левания и наличия диабетической нефропатии [40]. Более того, в исследовании Kim и соавт.…”

Section: Doi: 1014341/omet2017311-18unclassified

Fragility fractures and bone remodeling in type 2 diabetes mellitus

et al. 2017

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Fracture risk is significantly increased in both type 1 and type 2 diabetes and individuals with diabetes experience worse fracture outcomes compared to normoglycemic individuals. Patients with T1DM have decreased bone mineral density (BMD), whereas patients with T2DM demonstrate increased BMD compared to healthy control. The latest studies show increased incidence of low-traumatic fractures in patients with T2DM instead of high bone mineral density (BMD). The risk of osteoporotic fractures in patients with T2DM can be explained by disease complications and increased risk of falls and consequent trauma. However, the most important cause of bone fragility in T2DM is the deterioration in bone microarchitecture, the mechanism of which is not completely understood. High BMD in patients with T2DM does not allow us to use dual-energy X-ray-absorptiometry as a gold standard test for diagnosticsof osteoporosis. Consequently,new risk factors and diagnostic algorithm as well as treatment strategy should be developed for patients with T2DM. In addition to this, some researchers considered that the group of T2DM is geterogenous and physicians might face patients with osteoporosis and mild diabetes that add very little to bone fragility; patients with osteoporosis and moderate or severe diabetes which also affects bone tissue diabetoosteoporosis; and patients without osteoporosis but severe diabetes which cause bone tissue deterioration with the development of diabetic bone disease. New diagnostic tools and algorithm and new experimental research are needed for better understanding bone deterioration in patients with T2DM. This review summarizes our current knowledge on fracture rate, risk factors for fractures and causes of bone deterioration in subjects with T2DM.

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“…In a study performed on type 2 diabetic subjects with ages ranging between 26-94 years researchers concluded that serum vitamin D levels were inversely associated with HbA1c levels (r=−0.116, p=0.003). This relation maintains its independence in the multivariate analysis after adjusting for age, sex, HbA1c, body mass index, treatment and duration of diabetes and nephropathy (3).…”

Section: Introductionmentioning

confidence: 69%