Vitamin D deficiency in the aetiology of obesity‐related insulin resistance

Pramono, Adriyan; Jocken, Johan W. E.; Blaak, Ellen E.

doi:10.1002/dmrr.3146

Cited by 46 publications

(44 citation statements)

References 105 publications

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“…Specifically, OPA1 expression increased following vitamin D treatment, while mediators of mitochondrial fission (Fis1 and Drp1) were decreased (24) . Furthermore, current evidence has illustrated that treatment with 0•1 nM-1,25(OH) 2 D 3 in human primary muscle improved mitochondrial morphology (volume and structure) and altered mRNA expression of pyruvate dehydrogenase kinase 4 and carnitine palmitoyltransferase 1 (CPT1), important genes that control muscle glucose and lipid metabolism (86) . Vitamin D deficiency is known to impair muscle function and metabolism, where, in this case, skeletal muscle fibres are most likely to VDR ablation and to uptake cytoplasmic Ca 2þ released from the sarcoplasmic reticulum during twitch responses (87) .…”

Section: Mitochondrial Metabolismmentioning

confidence: 99%

Mechanisms of vitamin D action in skeletal muscle

et al. 2019

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Vitamin D receptor expression and associated function have been reported in various muscle models, including C2C12, L6 cell lines and primary human skeletal muscle cells. It is believed that 1,25-hydroxyvitamin D3 (1,25(OH)2D3), the active form of vitamin D, has a direct regulatory role in skeletal muscle function, where it participates in myogenesis, cell proliferation, differentiation, regulation of protein synthesis and mitochondrial metabolism through activation of various cellular signalling cascades, including the mitogen-activated protein kinase pathway(s). It has also been suggested that 1,25(OH)2D3 and its associated receptor have genomic targets, resulting in regulation of gene expression, as well as non-genomic functions that can alter cellular behaviour through binding and modification of targets not directly associated with transcriptional regulation. The molecular mechanisms of vitamin D signalling, however, have not been fully clarified. Vitamin D inadequacy or deficiency is associated with muscle fibre atrophy, increased risk of chronic musculoskeletal pain, sarcopenia and associated falls, and may also decrease RMR. The main purpose of the present review is to describe the molecular role of vitamin D in skeletal muscle tissue function and metabolism, specifically in relation to proliferation, differentiation and protein synthesis processes. In addition, the present review also includes discussion of possible genomic and non-genomic pathways of vitamin D action.

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Section: Mitochondrial Metabolismmentioning

confidence: 99%

Mechanisms of vitamin D action in skeletal muscle

et al. 2019

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“…In human population studies there is increasing evidence of a physiological role of vitamin D in glucose and lipid metabolism within insulin-sensitive tissues expressing VDR 17 . In adipose tissue (AT), vitamin D is thought to regulate markers of adipogenesis, such as adiponectin, as well as adipocyte apoptosis 18 .…”

Section: Introductionmentioning

confidence: 99%

Vitamin D deficiency serves as a precursor to stunted growth and central adiposity in zebrafish

Knuth

Mahapatra

Jima

et al. 2020

Sci Rep

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Emerging evidence demonstrates the importance of sufficient vitamin D (1α, 25-dihydroxyvitamin D3) levels during early life stage development with deficiencies associated with long-term effects into adulthood. While vitamin D has traditionally been associated with mineral ion homeostasis, accumulating evidence suggests non-calcemic roles for vitamin D including metabolic homeostasis. In this study, we examined the hypothesis that vitamin D deficiency (VDD) during early life stage development precedes metabolic disruption. Three dietary cohorts of zebrafish were placed on engineered diets including a standard laboratory control diet, a vitamin D null diet, and a vitamin D enriched diet. Zebrafish grown on a vitamin D null diet between 2–12 months post fertilization (mpf) exhibited diminished somatic growth and enhanced central adiposity associated with accumulation and enlargement of visceral and subcutaneous adipose depots indicative of both adipocyte hypertrophy and hyperplasia. VDD zebrafish exhibited elevated hepatic triglycerides, attenuated plasma free fatty acids and attenuated lipoprotein lipase activity consistent with hallmarks of dyslipidemia. VDD induced dysregulation of gene networks associated with growth hormone and insulin signaling, including induction of suppressor of cytokine signaling. These findings indicate that early developmental VDD impacts metabolic health by disrupting the balance between somatic growth and adipose accumulation.

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“…Low serum 25-hydroxyvitamin D (25(OH)D) levels are a common finding in the elderly population and are not limited to bone health risks, but also beta cell dysfunction and increased insulin resistance, leading to metabolic diseases [1][2][3]. However, a straightforward association between low serum 25(OH)D levels and cardiovascular diseases is not yet clear, especially in the elderly population which typically has more than one associated risk factor.…”

Section: Introductionmentioning

confidence: 99%

Vitamin D Deficient Older Adults Are More Prone to Have Metabolic Syndrome, but Not to a Greater Number of Metabolic Syndrome Parameters

et al. 2020

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This study investigated the relationship between metabolic parameters and low serum 25-hydroxyvitamin D (25(OH)D) levels in older adults (n = 265). They were assessed for anthropometrics and metabolic measurements, including 25(OH)D, insulin, glucose, total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (TG) and other inflammatory markers. Vitamin D deficiency was defined as a 25(OH)D level below 50 nmol/L. Comparisons between groups were performed using Wilcoxon–Mann–Whitney or Pearson’s Chi-squared test. A multivariate adjusted Poisson regression was used to model the number of metabolic parameters as a function of a set of explanatory variables. Subjects with 25(OH)D deficiency were predominantly females and presented higher body weight, body mass index, waist circumference, triglycerides and Tumor Necrosis Factor-α (TNF-α), and higher insulin resistance. Metabolic syndrome was also more prevalent among 25(OH)D-deficient subjects. In those without metabolic syndrome, 25(OH)D deficiency was related only to obesity and higher insulin resistance. Female sex, hypertension, higher waist circumference and higher levels of hemoglobin A1C (%), HDL-C, and TG were significantly associated with an increased number of metabolic syndrome parameters after adjusting for covariates, but 25(OH)D was not. The fact that serum 25(OH)D concentration was inversely associated with metabolic syndrome and insulin resistance not only reaffirms the relevance to consider serum 25(OH)D concentration as an influencing factor for insulin resistance, but also the need to actively screen for hypovitaminosis D in all patients with this condition.

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Vitamin D deficiency in the aetiology of obesity‐related insulin resistance

Cited by 46 publications

References 105 publications

Mechanisms of vitamin D action in skeletal muscle

Mechanisms of vitamin D action in skeletal muscle

Vitamin D deficiency serves as a precursor to stunted growth and central adiposity in zebrafish

Vitamin D Deficient Older Adults Are More Prone to Have Metabolic Syndrome, but Not to a Greater Number of Metabolic Syndrome Parameters

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