Vitamin D and Its Relationship with Obesity and Muscle

Cipriani, Cristiana; Pepe, Jessica; Piemonte, Sara; Colangelo, Luciano; Cilli, M.; Minisola, Salvatore

doi:10.1155/2014/841248

Cited by 81 publications

(58 citation statements)

References 106 publications

(128 reference statements)

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“…Changes in muscle morphology include derangement of the intermyofibrillar network, increases in intramuscular lipids, and atrophy of the fast‐twitch white (type 2) fibres,11, 44, 48, 49 which are the first to be recruited when preventing a fall. All these changes seem to be reversible,50 supporting co‐ordinated effects of vitamin D in musculoskeletal physiology 51, 52, 53, 54…”

Section: Vitamin D Physiologymentioning

confidence: 87%

Vitamin D, a modulator of musculoskeletal health in chronic kidney disease

Molina

Carrero

Bover

et al. 2017

J cachexia sarcopenia muscle

102

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The spectrum of activity of vitamin D goes beyond calcium and bone homeostasis, and growing evidence suggests that vitamin D contributes to maintain musculoskeletal health in healthy subjects as well as in patients with chronic kidney disease (CKD), who display the combination of bone metabolism disorder, muscle wasting, and weakness. Here, we review how vitamin D represents a pathway in which bone and muscle may interact. In vitro studies have confirmed that the vitamin D receptor is present on muscle, describing the mechanisms whereby vitamin D directly affects skeletal muscle. These include genomic and non‐genomic (rapid) effects, regulating cellular differentiation and proliferation. Observational studies have shown that circulating 25‐hydroxyvitamin D levels correlate with the clinical symptoms and muscle morphological changes observed in CKD patients. Vitamin D deficiency has been linked to low bone formation rate and bone mineral density, with an increased risk of skeletal fractures. The impact of low vitamin D status on skeletal muscle may also affect muscle metabolic pathways, including its sensitivity to insulin. Although some interventional studies have shown that vitamin D may improve physical performance and protect against the development of histological and radiological signs of hyperparathyroidism, evidence is still insufficient to draw definitive conclusions.

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Section: Vitamin D Physiologymentioning

confidence: 87%

Vitamin D, a modulator of musculoskeletal health in chronic kidney disease

Molina

Carrero

Bover

et al. 2017

J cachexia sarcopenia muscle

102

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“…It is possible that there may be a different set point for the calcium PTH relationship in the obese, as demonstrated in a calcium-citrate clamp that showed an exaggerated PTH response to hypocalcemia as compared to normal subjects (Hultin et al, 2010;Cipriani et al, 2014). Moreover, while many subjects with hypovitaminosis D could have PTH within the "normal" reference range, they may have "functional hyperparathyroidism" (Souberbielle et al, 2003).…”

Section: )mentioning

confidence: 99%

“…Growing evidence suggest larger doses of vitamin D (equivalent to 2000 IU to 10000 IU daily) are required to optimise vitamin D status (Vieth et al, 2007). Furthermore, the question what dose of vitamin D should be used in obese patients to replete vitamin D stores and how to maintain normal 25-OH D levels after repletion remains unresolved (Cipriani et al, 2014).…”

Section: Adequate Dose Of Vitamin Dmentioning

confidence: 99%

High Prevalence of Hypovitaminosis D in Postmenopausal Women with Type 2 Diabetes Mellitus

et al. 2016

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Abstract:The link between vitamin D and type 2 diabetes mellitus (T2DM) is intensively studied. This study aims to define the serum concentration of 25-hydroxyvitamin D (25-OH D) and to investigate the relationship between 25-OH D status, glycated hemoglobin (HbA1c) and body composition in postmenopausal women with T2DM and in non-diabetic controls. In this crosssectional study, 75 women with T2DM and 32 control subjects were selected. Serum 25-OH D, intact parathyroid hormone (PTH), calcium, fasting glucose and HbA1c, were measured. The mean 25-OH D level was 21.4 ± 11.4 ng/ml (range 4.1-50.7 ng/ml) in diabetic women and 30.3 ± 9.4 ng/ml (range 10.8-54.2 ng/ml) in control group (p<0.001). The prevalence of hypovitaminosis D (< 30 ng/ml) was higher in vitamin D 3 non-supplemented T2DM women (89% vs. 63% controls); the difference diminished in vitamin D 3 (500-1000 IU per day) supplemented subgroups (45% diabetics vs. 42% controls). In T2DM women, 25-OH D levels were not associated to HbA1c, duration of diabetes, fasting glucose and PTH levels, however, 25-OH D levels negatively associated with body mass index (p=0.011), total body fat mass (p=0.005) and total body lean mass (p=0.004). 6)Prague Medical Report / Vol. 117 (2016) No. 1, p. 5-17 of hypovitaminosis D is higher in non-supplemented postmenopausal women with T2DM than in non-diabetic controls (89% vs. 63%). Obesity is a risk factor for vitamin D insufficiency in T2DM postmenopausal women. Further studies evaluating relationships between fat, muscle, bone and vitamin D metabolism in T2DM patients are warranted.

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“…Interestingly, these fracture sites [7] differ from the fracture sites most commonly seen in osteoporosis, which are the wrist, upper arm, rib, hip and spine [7]. A number of possible contributors to compromised skeletal health in obesity have been proposed, including but not limited to reduced vitamin D bioavailability [9,14] and an inflammatory state that increases bone breakdown [15]. Moreover, individuals with obesity have a heightened risk of mobility impairment [16] and falls [17,18], due to factors such as poor compensatory stepping responses and postural instability [17] as well as intramuscular fat infiltration which reduces muscle strength [9,19,20].…”

Section: Introductionmentioning

confidence: 99%

Effects of obesity treatments on bone mineral density, bone turnover and fracture risk in adults with overweight or obesity

Harper

Pattinson

Fernando

et al. 2016

Hormone Molecular Biology and Clinical Investigation

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Background: New evidence suggests that obesity is deleterious for bone health, and obesity treatments could potentially exacerbate this. Materials and methods: This narrative review, largely based on recent systematic reviews and meta-analyses, synthesizes the effects on bone of bariatric surgery, weight loss pharmaceuticals and dietary restriction. Results and conclusions: All three obesity treatments result in statistically significant reductions in hip bone mineral density (BMD) and increases in bone turnover relative to pre-treatment values, with the reductions in hip BMD being strongest for bariatric surgery, notably Roux-en Y gastric bypass (RYGB, 8%-11% of pre-surgical values) and weakest for dietary restriction (1%-1.5% of pre-treatment values). Weight loss pharmaceuticals (orlistat or the glucagon-like peptide-1 receptor agonist, liraglutide) induced no greater changes from pre-treatment values than control, despite greater weight loss. There is suggestive evidence that liraglutide may increase bone mineral content (BMC) -but not BMD -and reduce fracture risk, but more research is required to clarify this. All three obesity treatments have variable effects on spine BMD, probably due to greater measurement error at this site in

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Vitamin D and Its Relationship with Obesity and Muscle

Cited by 81 publications

References 106 publications

Vitamin D, a modulator of musculoskeletal health in chronic kidney disease

Vitamin D, a modulator of musculoskeletal health in chronic kidney disease

High Prevalence of Hypovitaminosis D in Postmenopausal Women with Type 2 Diabetes Mellitus

Effects of obesity treatments on bone mineral density, bone turnover and fracture risk in adults with overweight or obesity

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