Does insulin resistance in type 2 diabetes alter vitamin D status?

2013 ◽  
Vol 7 (4) ◽  
pp. 283-287 ◽  
Author(s):  
Kamal Abdul Aziz Sulaiman Al-Shoumer ◽  
Adnan Ali Al-Asoosi ◽  
Aida Hussain Ali ◽  
Vasanthy Sudheer Nair
2021 ◽  
Vol Volume 14 ◽  
pp. 1393-1399
Author(s):  
Hang Zhao ◽  
Yong Tang ◽  
Chong Zheng ◽  
Luping Ren ◽  
Guangyao Song

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2651 ◽  
Author(s):  
Uwe Gröber ◽  
Michael F. Holick

The results of epidemiological and several interventional studies suggest an association between vitamin D deficiency and an increased risk of developing insulin resistance or type 2 diabetes. Various studies have indicated that a lack of vitamin D must be regarded as a pathogenic factor for type 2 diabetes and the metabolic syndrome, since a vitamin D deficiency (25(OH)D < 20 ng/mL) increases insulin resistance and reduces insulin secretion from beta cells in the pancreas. A recent study by Pittas et al. did not show a clear preventive effect of vitamin D supplementation with respect to the risk of developing type 2 diabetes. In terms of this study, it must be remembered that more than 70% of the participants in both the vitamin D supplement group and the placebo group did not have a vitamin D deficiency. In medical and pharmaceutical practice, more attention should be paid to vitamin D deficiency than has previously been accorded. Vitamin D status can be assessed objectively when necessary by laboratory testing of the serum 25(OH)D levels. Type 2 diabetes patients benefit from improving their vitamin D status with respect to their glucose metabolism and decreased mortality risk. Patients with insulin resistance who are vitamin D deficient should be treated with an appropriate amount of vitamin D to achieve circulating levels of 25(OH)D of 40–60 ng/mL.


2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Jie Zhang ◽  
Jianhong Ye ◽  
Gang Guo ◽  
Zhenhao Lan ◽  
Xing Li ◽  
...  

Objectives. Vitamin D deficiency plays a role in insulin resistance and the pathogenesis of type 2 diabetes mellitus. Little information is available about the association between vitamin D status and insulin resistance in the Chinese population. Currently, vitamin D status is evaluated by the concentrations of serum 25-hydroxyvitamin D [25(OH)D]. This study explores the relationship between insulin resistance and serum 25-hydroxyvitamin D concentrations in Chinese patients with type 2 diabetes mellitus.Subjects and Methods. This study included 117 patients with type 2 diabetes. The following variables were measured: 25-hydroxyvitamin D [25(OH)D], glycosylated hemoglobin A1c (HbA1c), fasting blood glucose (FBS), fasting blood insulin (FINS), fasting blood C-peptide, serum creatinine (SCr), glomerular filtration rate (eGFR), body mass index (BMI), and homeostatic model estimates of insulin resistance (HOMA-IR).Results. The cases were divided into three groups: Group 1 (G1) with 25(OH)D ≤ 20 ng/mL [≤50 nmol/L], Group 2 (G2) with 25(OH)D values from 20 ng/mL [50 nmol/L] to 30 ng/mL [75 nmol/L], and Group 3 (G3) with 25(OH)D ≥ 30 ng/mL [≥75 nmol/L], with 52.6%, 26.3%, and 21.1% of subjects in Groups 1–3, respectively. There was a negative correlation between 25(OH)D and HOMA-IR (β= −0.314,p=0.001) adjusted by age, BMI, and eGFR.Conclusion. Better vitamin D status may be protective of glucose homeostasis since 25(OH)D was negatively associated with insulin resistance in Chinese patients with type 2 diabetes.


2005 ◽  
Vol 18 (2) ◽  
pp. 175-182 ◽  
Author(s):  
Mario Flores

Evidence from different directions, including observational and experimental studies, points to a role of vitamin D status in low-intensity chronic inflammation and insulin resistance in type 2 diabetes mellitus (T2DM). It has been recognised that insulin resistance and low-intensity chronic inflammation are risk factors for T2DM. Thus, vitamin D status can be implicated in the aetiology of TD2M. It is suggested that the relationship between vitamin D and low-intensity chronic inflammation and insulin resistance in T2DM can be mediated in part by the immune-modulating properties of the active form of vitamin D (1-α,25-dihydroxyvitamin D3; 1,25(OH)2D3), which is able to down regulate the production of pro-inflammatory cytokines – particularly TNF-α, and IL-6. However, an association between vitamin D status and these features, which is independent of BMI, has been also reported. Non-calcaemic effects of vitamin D can be associated with health outcomes other than those traditionally attributed to the vitamin.


Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 588-P
Author(s):  
ANI S. TODOROVA ◽  
RUMYANA DIMOVA ◽  
NEVENA CHAKAROVA ◽  
MINA SERDAROVA ◽  
GRETA GROZEVA-DAMYANOVA ◽  
...  

2021 ◽  
Vol 22 (12) ◽  
pp. 6444
Author(s):  
Anna Gabryanczyk ◽  
Sylwia Klimczak ◽  
Izabela Szymczak-Pajor ◽  
Agnieszka Śliwińska

There is mounting evidence that type 2 diabetes mellitus (T2DM) is related with increased risk for the development of cancer. Apart from shared common risk factors typical for both diseases, diabetes driven factors including hyperinsulinemia, insulin resistance, hyperglycemia and low grade chronic inflammation are of great importance. Recently, vitamin D deficiency was reported to be associated with the pathogenesis of numerous diseases, including T2DM and cancer. However, little is known whether vitamin D deficiency may be responsible for elevated cancer risk development in T2DM patients. Therefore, the aim of the current review is to identify the molecular mechanisms by which vitamin D deficiency may contribute to cancer development in T2DM patients. Vitamin D via alleviation of insulin resistance, hyperglycemia, oxidative stress and inflammation reduces diabetes driven cancer risk factors. Moreover, vitamin D strengthens the DNA repair process, and regulates apoptosis and autophagy of cancer cells as well as signaling pathways involved in tumorigenesis i.e., tumor growth factor β (TGFβ), insulin-like growth factor (IGF) and Wnt-β-Cathenin. It should also be underlined that many types of cancer cells present alterations in vitamin D metabolism and action as a result of Vitamin D Receptor (VDR) and CYP27B1 expression dysregulation. Although, numerous studies revealed that adequate vitamin D concentration prevents or delays T2DM and cancer development, little is known how the vitamin affects cancer risk among T2DM patients. There is a pressing need for randomized clinical trials to clarify whether vitamin D deficiency may be a factor responsible for increased risk of cancer in T2DM patients, and whether the use of the vitamin by patients with diabetes and cancer may improve cancer prognosis and metabolic control of diabetes.


Author(s):  
Ani S. Todorova ◽  
Edward B. Jude ◽  
Rumyana B. Dimova ◽  
Nevena Y. Chakarova ◽  
Mina S. Serdarova ◽  
...  

The aim of this study was to assess vitamin D status in patients with type 2 diabetes and diabetic foot ulcers (DFU). A total of 242 participants with type 2 diabetes, mean age 59.1 ± 10 years, mean body mass index 31.4 ± 6.3 kg/m2, and estimated glomerular filtration rate ≥45 mL/min/1.73m2, were divided into 2 groups: 73 with DFU (35 with and 38 without active infection) and 169 without DFU (106 with diabetic peripheral neuropathy, 63 without complications). Neuropathy was assessed by 10 g monofilament, Rydel-Seiffer 128 Hz tuning fork, and temperature discrimination. Serum 25(OH)D (25-hydroxy vitamin D) was assessed by ECLIA (electro-chemiluminescence immunoassay) method. Median 25(OH)D level was 12.6 ng/mL (IQR [interquartile range] 9.3-17.6 ng/mL) in the studied cohort. The DFU group presented with lower 25(OH)D level as compared with diabetic patients without foot ulcers (non-DFU group): 11.6 ng/mL (IQR 8.5-15.8 ng/mL) versus 13.5 ng/mL (IQR 9.6-18.6 ng/mL), P = .001; the diabetic peripheral neuropathy subgroup demonstrated lower 25(OH)D level in comparison with participants without complications: 12.5 ng/mL (IQR 9-17.2 ng/mL) versus 15.9 ng/mL (IQR 10.4-20.8 ng/mL), P = .031. This remained significantly different even after correction for age and duration of diabetes. There was no difference in 25(OH)D level between the subgroups according to the presence of active infection. In conclusion, vitamin D deficiency may play a role in the development of diabetes complications.


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