Low Vitamin D Levels in Northern American Adults with the Metabolic Syndrome

Devaraj, Sridevi; Jialal, Ganesh; Cook, T.J; Siegel, David M.; Jialal, Ishwarlal

doi:10.1055/s-0030-1268485

Cited by 58 publications

(51 citation statements)

References 8 publications

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“…82,89,90 Another finding, which further corroborated the in-verse correlation of 25-(OH)D with metabolic disease/ diabetes in our analysis, was the negative association between 25-(OH)D levels and HbA1c values. This inverse association is supported by other published reports 20,[91][92][93] and the seasonal variation of 25-(OH) D levels is inversely mirrored by HbA1c, with the lowest levels observed in the summer. 94 Indeed, low levels of 25-(OH)D are considered a risk factor for the development of insulin resistance and diabetes, 4,95 although the preventive effect of VitD supplementation has not yet been fully established.…”

Section: 55supporting

confidence: 84%

Vitamin D levels in a large Mediterranean cohort: reconsidering normal cut-off values

Katrinaki

Kampa

Margioris

et al. 2016

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Section: 55supporting

confidence: 84%

Vitamin D levels in a large Mediterranean cohort: reconsidering normal cut-off values

Katrinaki

Kampa

Margioris

et al. 2016

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“…They have a very short half-life, which is further reduced under conditions of stress [34,35,36]. Thus an increase in the total CD11c+ cells in a tissue would most probably be due to cells migrating from the periphery.…”

Section: Discussionmentioning

confidence: 99%

Recruitment and in situ Renewal Regulate Rapid Accumulation of CD11c+ Cells in the Lung following Intranasal Superantigen Challenge

Muralimohan

Rossi²,

Vella³

2008

Int Arch Allergy Immunol

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Background: Staphylococcusaureus, a primary source of bacterial superantigen, is known to colonize the human respiratory tract and has been implicated in airway inflammation. The potential pathological effect of staphylococcal enterotoxins on the respiratory tract necessitates a detailed understanding of how they regulate innate immune cells, particularly CD11c-expressing dendritic cells (DCs). Methods: C57BL/6 mice were challenged intranasally with staphylococcal enterotoxin A (SEA) and at indicated time points lung tissue was perfused, digested and analyzed for CD11c+ expressing cells. Results: The pulmonary CD11c+ cells can be divided into two major populations based on their MHC II expression. One day following intranasal SEA challenge, there was rapid accumulation of CD11c+ cells expressing medium to high levels of MHC II. The peak accumulation of CD11c+ MHC II– population was observed 2 days after SEA challenge; however, careful examination of this cell population revealed that they were heterogeneous, being comprised of cells bearing CD3, CD19, NK1.1 and F4/80 along with varying levels of CD11c. Nevertheless, there was a 2-fold increase of CD11c+ MHC II– (CD3– CD19– NK1.1– F4/80–) cells in the lungs. Conclusion: The mechanism of increase in the CD11c+ MHC II– immune progenitor population was mainly due to cellular division rather than migration from blood to lung. In contrast, the early and rapid accumulation of CD11c+ MHC II^hi cells, conventionally known as DCs, in the lung on day 1 was mostly due to migration from blood. Thus this study examines the pulmonary innate immune response to a powerful immune stimulus.

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“…In fact following supplementation his most recent PTH level is now 34 pg/ml. Also we have previously reported low Vitamin D levels with values below 20 ng/ml in 30% of patients with Metabolic Syndrome and 8% of controls [4] . In that study we had no obvious explanation since there was no drug causes and all patients had normal renal and hepatic function however like in the present patient the average BMI was consistent with obesity (30.1 in controls and 35.1 in patients with Metabolic Syndrome).…”

Section: Discussionmentioning

confidence: 72%

Vitamin D deficiency of unknown etiology

Jialal

Allen

2015

CRCP

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We report on a 68-year-old Caucasian male who was referred to our Metabolic Clinic with a very low 25 hydroxy-vitamin D (25(OH)D) level of 4.0 ng/ml. History did not reveal any medications know to interfere with 25(OH)D metabolism or history of bone pains or weakness and clinical examination did not reveal myopathy. Relevant laboratory testing confirmed the low 25(OH)D with hypocalcinuria. All other laboratory tests were essentially normal. He was started on oral Vitamin D supplementation and had an excellent response with his most recent level at 35.1 ng/ml. Since we could not find an obvious cause for his Vitamin D deficiency we speculate that it is possibly due to his obesity and suggest that obese persons be screened for Vitamin D deficiency. Key wordsVitamin D, Parathyroid hormone, Malabsorption, Obesity, Calcium Case presentationA 68-year-old Caucasian male was referred to the Metabolic Clinic at the Veterans Affairs Medical Center for management of Vitamin D deficiency. When he was referred he had a 25 hydroxyvitamin D (25(OH)D) level of 4.0 ng/ml. Vitamin D deficiency is defined as a level < 20 ng/ml [1] . History did not reveal any muscle weakness and he was not taking any medications know to interfere with Vitamin D metabolism such as anticonvulsants, glucocorticoids, medications for AIDS etc. Also he did not admit to any symptoms of malabsorption and was eating a normal diet and obtaining adequate sun exposure living in Northern California. His past history was positive for hypertension and osteoarthritis. The medications he was taking included amlodipine 10 mg/d and hydrochlorthiazide 25 mg, triamaterene 37.5 mg/d. Physical examination revealed a normal healthy male with a weight of 181 lbs a body mass index of 30.2 kg/m 2 a BP of 130/70, with normal cardiac and chest examinations. Also he had no evidence of proximal myopathy. As shown in Table 1 he has calcium, phosphate and alkaline phosphatase levels in the reference ranges. His 24 hour urine calcium was decreased. He had a normal urinalysis, serum creatinine and liver function tests. Both Parathyroid hormone (PTH) and 1.25 dihydroxy Vitamin D levels were normal. His DEXA scan revealed normal bone mineral density. Furthermore he had a normal hemoglobin of 17.1 (14 g/dl -18 g/dl), percent iron saturation of 43% (11%-46%) and a ferritin of 289 (22 ng/ml -415 ng/ml). Also Vitamin A levels were normal 51 (18 µg/dl -77 µg/dl). Screening for celiac disease revealed normal titers of tissue transglutaminase and endomysial antibodies. His repeat 25(OH)D level was 14 ng/ml (Supplement use could not be ruled out at this stage). Based on his low 25(OH)D levels and decreased urinary calcium excretion a diagnosis

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Low Vitamin D Levels in Northern American Adults with the Metabolic Syndrome

Cited by 58 publications

References 8 publications

Vitamin D levels in a large Mediterranean cohort: reconsidering normal cut-off values

Vitamin D levels in a large Mediterranean cohort: reconsidering normal cut-off values

Recruitment and in situ Renewal Regulate Rapid Accumulation of CD11c+ Cells in the Lung following Intranasal Superantigen Challenge

Vitamin D deficiency of unknown etiology

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