SciELO - Scientific Electronic Library Online

vol.30 número6Cambios en puntos temporales específicos en ADN-metiltransferasas en relación con el promotor de leptina durante el desarrollo de obesidadAnálisis comparativo de la respuesta glicémica e índice glicémico del puré de papas instantáneo determinado en sujetos sometidos a gastrectomía vertical en manga laparoscópica y en sujetos controles índice de autoresíndice de materiabúsqueda de artículos
Home Pagelista alfabética de revistas  

Servicios Personalizados




Links relacionados

  • En proceso de indezaciónCitado por Google
  • No hay articulos similaresSimilares en SciELO
  • En proceso de indezaciónSimilares en Google


Nutrición Hospitalaria

versión On-line ISSN 1699-5198versión impresa ISSN 0212-1611

Nutr. Hosp. vol.30 no.6 Madrid dic. 2014 

ORIGINAL / Obesidad


Vitamin D levels and bone turnover markers are not related to non-alcoholic fatty liver disease in severely obese patients

Los niveles de vitamina D y marcadores de recambio óseo no se encuentran relacionados con el hígado graso no alcohólico en obesos mórbidos



Rubén Díez Rodríguez1,2, María D. Ballesteros Pomar1,3, Alicia Calleja Fernández1-3, Sara Calleja Antolín1,4, Isidoro Cano Rodríguez1,3, Pedro Linares Torres2, Francisco Jorquera Plaza2 and José Luis Olcoz Goñi1,2

1High Risk Obesity Unit, Complejo Asistencial Universitario de León.
2Digestive Disease Department, Complejo Asistencial Universitario de León.
3Endocrinology and Nutrition Department, Complejo Asistencial Universitario de León.
4Immunology Department, Complejo Asistencial Universitario de León. León, Spain.

This study was part of a project funded by the Health Department of Castilla y Leon (SACYL), Spain. Biomedicine Biotechnology and Health science project. PROJECT GRS 401/A/09.





Background: Morbidly obese patients usually present vitamin D deficiency or secondary hyperparathyroidism. Low vitamin D levels have been recently related to non-alcoholic fatty liver disease (NAFLD). The aim of this study was to analyse the relationship between vitamin D, bone turnover markers and non-alcoholic fatty liver disease and metabolic syndrome in severely obese patients.
Methods: One hundred and ten patients who underwent bariatric surgery were included. Liver biopsy was taken during surgery. Two univariate analyses were carried out in order to i) analyse the relationship between liver histology and vitamin D-bone turnover markers (intact parathyroid hormone (PTH), osteocalcin and Carboxy-terminal collagen crosslinks) and ii) establish the association between metabolic syndrome components-insulin resistance (HOMA) and vitamin D-bone turnover markers.
Results: 70% of the patients had lower levels of vitamin D or secondary hyperparathyroidism. None of the components of liver histology were associated with levels of vitamin D or with bone turnover parameters. Patients with metabolic syndrome showed lower levels of PTH and osteocalcin (72,42 (29,47) vs 61.25(19.59) p-Value: 0.022; 19.79 (10.43) vs 16.87(10.25) p-Value: 0,028, respectively). HOMA was not related to Vitamin D or bone turnover markers.
Conclusion: Low levels of vitamin D or hyperparathyroidism are common in severely obese patients. Vitamin D and bone metabolism markers were associated neither to NAFLD nor with metabolic syndrome in our series of obese morbid patients.

Key words: Vitamin D Deficiency. Morbid obesity. Non alcoholic fatty liver Disease.


Antecedentes: los pacientes con obesidad mórbida presentan frecuentemente déficit de vitamina D o hiperparatiroidismo secundario. Presentar niveles bajos de vitamina D se ha asociado recientemente con el hígado graso no alcohólico (EHNA). El objetivo de este estudio fue analizar la relación de la vitamina D y los marcadores de recambio óseo con el hígado graso no alcohólico y el síndrome metabólico, en pacientes con obesidad mórbida.
Métodos: Ciento diez pacientes sometidos a cirugía bariátrica fueron incluidos, obteniéndose una biopsia hepática durante la cirugía. Dos análisis univariados se llevaron a cabo con el fin de: i) analizar la relación de la histología hepática con la vitamina D y marcadores de recambio óseo (hormona paratiroidea intacta (PTH), osteocalcina y enlaces cruzados de colágeno carboxi-terminal) y ii) establecer la asociación de los componentes del síndrome metabólico y resistencia a la insulina (HOMA) con los marcadores de recambio óseo y vitamina D.
Resultados: El 70% de los pacientes presentaron niveles bajos de vitamina D o hiperparatiroidismo secundario. Ninguno de los componentes de la histología hepática resultó asociado con los niveles de vitamina D o con los parámetros de recambio óseo. Los pacientes con síndrome metabólico mostraron un nivel menor de PTH (72,42 (29,47) vs 61,25 (19,59) Valor p: 0.022) y de osteocalcina 19,79 (10,43) vs 16,87 (10,25) p-valor: 0.028). El HOMA no resultó relacionado con la vitamina D o con los marcadores de recambio óseo.
Conclusión: Niveles bajos de vitamina D e hiperparatiroidismo secundario son hallazgos frecuentes en pacientes con obesidad mórbida en nuestro medio. Los marcadores de la vitamina D y recambio óseo no resultaron asociados con el hígado graso no alcohólico, ni con el síndrome metabólico en nuestra serie de pacientes obesos mórbidos.

Palabras clave: Deficit de vitamina D. Obesidad mórbida. Hígado graso no alcohólico.

ALT: Alanine transaminase.
AST: Aspartate aminotransferase.
BMI: Body mass index.
DM: Diabetes Mellitus.
CRP: C reactive protein.
CTX: Carboxy-terminal collagen crosslinks.
GGT: Gamma-Glutaryl transferase.
HBP: High blood pressure.
HOMA: Homeostasis model assessment.
IR: Insulin resistance.
MS: Metabolic syndrome.
NAFLD: Non-alcoholic fatty liver disease.
NASH: Non-alcoholic steatohepatitis.
PTH: Intact parathyroid hormone.
Vit D 25: 25-hydroxyvitamin D.
WC: Waist circumference.



Vitamin D is essential to the regulation of the osteometabolic system, but it has other extra skeleton effects. Several evidences have shown that vitamin D deficient individuals are more likely to develop glucose intolerance, metabolic syndrome and type 2 diabetes mellitus1, and also Vitamin D levels have been related to cardiovascular disease2,3.

The prevalence of hypovitaminosis D in adult population is about 30-60%4,5 and in severely obese patients decreased levels of Vitamin D have been reported in 80% of the cases6. The relationship between obesity and vitamin D remains unclear. It may have a multifactorial etiology: suboptimal synthesis (inadequate sun exposure or less exercise due to reduced mobility), increased storage of vitamin D in adipose tissue, and impaired production of 25-hydroxyvitamin in the liver because of hepatic steatosis7,8. A recent study suggests that vitamin D deficiency is associated with increased risk of developing obesity5.

The prevalence of non-alcoholic fatty liver disease (NAFLD) in patients undergoing bariatric surgery exceeds 90%9,10 and the range of prevalence of non-alcoholic steatohepatitis (NASH) in obese population was 10-56 %11. NAFLD has been associated to insulin resistance, metabolic syndrome and diabetes, but the reason to progress from simple steatosis to NASH or cirrhosis remains unclear. A multi-hit hypothesis has been proposed, where multiple factors (nutritional, genetic factors mainly) might contribute to liver inflammation development12.

Decreased levels of Vitamin D have been related to NAFLD13, so vitamin D deficiency is thought to play a role in the development of NALFD and in the progression of liver inflammation14. Less information about the role of intact parathyroid hormone (PTH) levels and bone turnover markers in NALFD has been reported.

The relationship between vitamin D, bone turnover markers and NAFLD has not been evaluated in morbidly obese patients, so the aim of this study was to analyse the relationship between vitamin D and bone turn over markers, non-alcoholic liver disease and metabolic syndrome in severely obese patients candidates to undergo bariatric surgery.


Material and methods


Patients who underwent bariatric surgery at third level hospital between June 2008 and March 2013 were prospectively included. The patients were included if they fulfilled SEEDO (Spanish Society for Obesity study) criteria for bariatric surgery15: body mass index (BMI) above 40 kg/m2 or above 35 kg/m2 with obesity associated comorbidities. Scopinaro's laparoscopic biliopancreatic diversion was performed and a liver biopsy was obtained during surgery.

The exclusion criteria were: patients with primary hyperparathyroidism or renal disease, alcohol intake higher than 20g/day and other causes of liver disease (Hepatitis C, hepatitis B, autoimmune liver disease, hemochromatosis and treatment with steatosis inducing drugs). The study was approved by the Clinical research ethics committee in our hospital and written informed consent was obtained from all patients.

Clinical and laboratory

Clinical and anthropometric data were collected 2-4 weeks before surgery. Body mass index (BMI) was calculated using the following equation: Weight (Kg)/ height (meters)2. Waist circumference (WC) was measured at the midpoint between the lower border of the rib cage and the iliac crest.

The diagnosis of type 2 diabetes was based on the criteria of the American Diabetes Association, using a value of fasting blood glucose ≥ 126mg/dL at least twice16. The diagnosis of high blood pressure (HBP) was based on the following criteria: systolic blood pressure ≥135mmHg, and diastolic ≥85mmHg measured, at least, three times. Metabolic syndrome (MS) was diagnosed according ATPIII criteria17.

A 8 hour-overnight fasting blood sample was obtained as a part of preoperative routine study to measure serum levels of: 25-hydroxyvitamin D (vit D 25) (ng/ mL), intact parathyroid hormone (PTH) (pg/mL), osteocalcin, Carboxy-terminal collagen crosslinks (CTX) (ng/mL), alanine transaminase (ALT) (UI/L), aspartate aminotransferase (AST) (UI/L), Gamma-Glutaryl transferase (GGT) (UI/L), total cholesterol (mg/dL), HDL-cholesterol (mg/dL), triglycerides (mg/dL), glucose (mg/dL) and insulin μU/mL). VitD 25 was measured by electro immunochemoluminescence, CTX by enzyme-linked immunosorbent assay, Osteocalcin by radioimmuno assay and PTH by immunochemo-luminescence. Insulin resistance (IR) was determined by homeostasis model assessment (HOMA) using the following equation: fasting insulin μU/ml) x fasting glucose (mmol/L)/22.5).

Secondary hyperparathyroidism and vitamin D deficiency were considered whenever PTH levels were above 72 pg/ml, and VitD 25 ≤ 20 ng/ml, according to Endocrine Society recommendation18.


A liver biopsy of at least 15 mm was obtained during surgery to ensure that it was feasible19, and analysed by an expert pathologist. The Kleiner classification was used to establish NAS score (from 0 to 8), including steatosis (0 to 3), lobular inflammation (0 to 3) and hepatocellular ballooning (0 to 2). Fibrosis stage was classified from 0-420. NASH was considered if NAS score was ≥5, not NASH if NAS score 0-2, and indeterminate if 3-4.


Continuous variables were expressed as mean (standard deviation), and categorical variables as frequency (percentage). A p-Value < 0.05 was considered as significant. Statistical analysis was performed using SPSS 15.0 for Windows.

The normality of the distribution was determined by the Kolmogorov-Smirnov test. Before statistical analysis, skewed variables (vitamin D, HOMA, PTH, osteocalcin, CTX) were logarithmically transformed to improve normality. In text and tables these variables are represented in their natural units.

Two univariate analyses were carried out to valuate the relationships between i) liver histology and vitamin D-bone turnover markers and ii) between metabolic syndrome components and vitamin D-bone turnover markers. For a quantitative predictor and more than two levels of exposure variables, analysis of variance (ANOVA) was applied. Student t-test was used to compare two means or U the Mann- Whitney if they did not follow a normal distribution. Chi-squared or Fisher exact test were used for qualitative predictor. Pearson correlation coefficient was utilised to study the relationship between two continuous variables.



From the 136 patients analysed, 26 were excluded because vitamin D, PTH levels or bone turnover markers data were not available. Patient's characteristics and pathological features are shown in table I and II, respectively. 48.2% (53/110) had HBP, 28.1% (24/110) DM and 48.2% met criteria for metabolic syndrome. 33.6% (37/110) had hyperparathyroidism, and 60.9%(67/110) vitamin D deficiency. 30% (33/110) of the patients had neither hyperparathyroidism nor vitamin D deficiency.




Table III shows the relationship between liver histology, vitamin D levels and bone metabolism. None of the analysed parameters were related to liver histology. In table IV, the analysis between vitamin D, bone metabolism, metabolic syndrome and other features are represented. Patients with MS had lower levels of PTH (61.25 vs 72.42, p-Value 0.022) and lower levels of osteocalcin (16.87 vs 19.79, p-Value 0.028).

Attending to NAS score, the distribution of patients with vitamin D deficiency was: NAS score 0-2: 40/63(63.5%); NAS score 2-4: 14/29(48.3%); NAS score≥ 5: 12/18(66.7%), p-Value: 0.314; and the distribution of patients with hyperparathyroidism was: NAS score 0-2: 22/63(34.5%); NAS score 2-4: 9/29(31%); NAS score ≥ 5: 6/18(33.3%), p-Value:0.935.

Patients with vitamin D deficiency or with hyperparathyroidism did not show statistically significant higher HOMA levels (Vitamin D deficiency: 6.79(4.52) vs Non-Vitamin D deficiency: 5.81(3.36), p-Value: 0.328; hyperparathyroidism: 5.71(3.82) vs Non-Hyperparathyroidism: 6.75 (6.75), p-Value: 0.209). Hypovitaminosis D was present in 58.5%(31/53) of patients with MS and in 61.4%(35/57) of the patients without MS (p-Value 0.76); hyperparathyroidism was observed in the 24.5%(13/53) of patients with MS and in the 41.2%(24/57) of the patients without MS (p-Value 0.051).



This cross-sectional study presents a novel approach to establish the relationship between vitamin D, bone turnover markers, metabolic syndrome and liver histology in obese patients candidates to bariatric surgery.

Nonetheless, this study has several limitations. Firstly, as this is not a controlled study and a cross-sectional design is used, results should be interpreted with caution. A control group of non severely obese patients with and without NAFLD would be needed to establish the role of morbid obesity in the co-relation between NAFLD and vitamin D levels. Moreover, the study did not take into account the season in which the levels of vitamin D were measured or the treatment with supplements of calcium and vitamin D.

In our study, higher levels of vitamin D were found among patients with normal biopsy, without NASH or without fibrosis, although the differences are not statistically significant. The low prevalence of NASH and high prevalence of low vitamin D levels in our environment could explain the difficulty to achieve statistical significance.

The relationship between NAFLD and vitamin D remains unclear. A recent meta-analysis observed that NAFLD patients were 1.26 times more likely to be vitamin D deficient (95% CI: 1.17-1.35)14, but some studies did not find association between NAFLD and Vitamin D levels21,22. Only in four of the seventeen studies included in the meta-analysis, NAFLD was diagnosed by liver biopsy.

The pathogenesis of the association between NA-FLD and vitamin D is not well explained. Evidences from animal studies support the hypothesis of an immunomodulatory role of vitamin D in NAFLD. Vitamin D deficient diet could produce expression of increased hepatic mRNA levels of IL-4, IL-6 or TNFα23. Moreover, phototherapy in animal models elevated vitamin D levels and could improve insulin resistance and reduce liver inflammation24. A recent controlled clinical trial patients with NAFLD showed no differences in liver function test, HOMA and grade of steatosis in ultrasound after four months of oral supplementation with vitamin D25.

Osteocalcin has been related to insulin resistance and liver fibrosis26. Patients with chronic liver disease show low levels of osteocalcin, but relationship among these parameters has not been clarified yet27. Lee et al28 demonstrated that osteocalcin participates in adiposity and glucose homeostasis, suggesting skeleton influences on energy metabolism, so osteocalcin could be a surrogate marker of insulin resistance26. The relationship between osteocalcin and metabolic syndrome observed in our cohort, does not support this fact.

The association of vitamin D and PTH with metabolic syndrome also remains unclear. Some evidences support the association of PTH levels with metabolic syndrome based on the relationship between PTH and insulin resistance29,30, but other studies have shown that PTH were not related to metabolic syndrome after adjust of vitamin D levels31,32. The co-relation between vitamin D deficiency and MS is supported by data from several observational studies, but the pathogenesis is not well defined and vitamin D supplementation in MS patients does not improve metabolic parameters33. In our cohort, PTH levels were inversely correlated to the presence of metabolic syndrome and vitamin D was not associated with metabolic syndrome.

Moreiro et al34 found that 58% of the patients with normal presurgery PTH levels, after two years of Scopinaro's Biliopancreatic diversion, developed secondary hyperparathyroidism in spite of calcium and vitamin D supplementation. Alvarez et al35 observed hypovitaminosis D after an average of 26 months of a Sleeve gastrectomy in 43% of patients and 8% hyperparathyroidism. In our series 34% of the patients showed hyperparathyroidism, and 61% vitamin D deficiency. Checking vitamin D and PTH levels in severely obese patients presurgery is mandatory due to the high prevalence of vitamin D deficiency or secondary hyperparathyroidism observed.



In our cohort of severely obese patients, vitamin D and bone metabolism markers were associated neither to NAFLD nor with metabolic syndrome. About 70% of our obese patients showed low levels of vitamin D or hyperparathyroidism, so this should be tested pre-surgery and treated. Further research is needed to establish the relationship between NAFLD and vitamin D levels in severely obese patients.



1. Hjelmesaeth J, Hofso D, Aasheim ET, Jenssen T, Moan J, Hager H, et al. Parathyroid hormone, but not vitamin D, is associated with the metabolic syndrome in morbidly obese women and men: a cross-sectional study. Cardiovasc Diabetol 2009;8:7.         [ Links ]

2. Kendrick J, Targher G, Smits G, Chonchol M. 25-Hydroxyvitamin D deficiency is independently associated with cardiovascular disease in the Third National Health and Nutrition Examination Survey. Atherosclerosis 2009;205(1):255-60.         [ Links ]

3. Anderson JL, May HT, Horne BD, Bair TL, Hall NL, Carlquist JF, et al. Relation of vitamin D deficiency to cardiovascular risk factors, disease status, and incident events in a general healthcare population. The American journal of cardiology 2010;106(7):963-8.         [ Links ]

4. Targher G, Byrne CD. Lower 25-hydroxyvitamin D3 levels and increased risk of liver diseases: is there a causal link? Endocrine 2014.         [ Links ]

5. Gonzalez-Molero I, Rojo-Martinez G, Morcillo S, Gutierrez C, Rubio E, Perez-Valero V, et al. Hypovitaminosis D and incidence of obesity: a prospective study. European journal of clinical nutrition 2013;67(6):680-2.         [ Links ]

6. Ybarra J, Sanchez-Hernandez J, Gich I, De Leiva A, Rius X, Rodriguez-Espinosa J, et al. Unchanged hypovitaminosis D and secondary hyperparathyroidism in morbid obesity after bariatric surgery. Obesity surgery 2005;15(3):330-5.         [ Links ]

7. Wortsman J, Matsuoka LY, Chen TC, Lu Z, Holick MF. Decreased bioavailability of vitamin D in obesity. The American journal of clinical nutrition 2000;72(3):690-3.         [ Links ]

8. Earthman CP, Beckman LM, Masodkar K, Sibley SD. The link between obesity and low circulating 25-hydroxyvitamin D concentrations: considerations and implications. Int J Obes (Lond). 2012;36(3):387-96.         [ Links ]

9. Chalasani N, Younossi Z, Lavine JE, Diehl AM, Brunt EM, Cusi K, et al. The diagnosis and management of non-alcoholic fatty liver disease: practice guideline by the American Gastroenterological Association, American Association for the Study of Liver Diseases, and American College of Gastroenterology. Gastroenterology 2012;142(7):1592-609.         [ Links ]

10. Ballesteros Pomar M, Urioste Fondo A, Gonzázez de Francisco T, Olcoz Goñi J, González Herraez L, Bailador C, et al. Prevalence and predictors of Non-Alcoholic Fatty liver Disease (NAFLD) in morbidly obese patients undergoing bariatric surgery. Int J Obes (Lond). 2007(31):S133.         [ Links ]

11. Vernon G, Baranova A, Younossi ZM. Systematic review: the epidemiology and natural history of non-alcoholic fatty liver disease and non-alcoholic steatohepatitis in adults. Aliment Pharmacol Ther 2011;34(3):274-85.         [ Links ]

12. Tilg H, Moschen AR. Evolution of inflammation in nonalcoholic fatty liver disease: the multiple parallel hits hypothesis. Hepatology 2010;52(5):1836-46.         [ Links ]

13. Barchetta I, Angelico F, Del Ben M, Baroni MG, Pozzilli P, Morini S, et al. Strong association between non alcoholic fatty liver disease (NAFLD) and low 25(OH) vitamin D levels in an adult population with normal serum liver enzymes. BMC medicine 2011;9:85.         [ Links ]

14. Eliades M, Spyrou E, Agrawal N, Lazo M, Brancati FL, Potter JJ, et al. Meta-analysis: vitamin D and non-alcoholic fatty liver disease. Aliment Pharmacol Ther 2013;38(3):246-54.         [ Links ]

15. Salas-Salvado J, Rubio MA, Barbany M, Moreno B. SEEDO 2007 Consensus for the evaluation of overweight and obesity and the establishment of therapeutic intervention criteria. Medicina clinica 2007;128(5):184-96; quiz 1 p following 200.         [ Links ]

16. Executive summary: Standards of medical care in diabetes--2013. Diabetes Care 2013;36 Suppl 1:S4-10.         [ Links ]

17. Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). JAMA: the journal of the American Medical Association 2001;285(19):2486-97.         [ Links ]

18. Holick MF, Binkley NC, Bischoff-Ferrari HA, Gordon CM, Hanley DA, Heaney RP, et al. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society clinical practice guideline. The Journal of clinical endocrinology and metabolism 2011;96(7):1911-30.         [ Links ]

19. Colloredo G, Guido M, Sonzogni A, Leandro G. Impact of liver biopsy size on histological evaluation of chronic viral hepatitis: the smaller the sample, the milder the disease. J Hepatol 2003;39(2):239-44.         [ Links ]

20. Kleiner DE, Brunt EM, Van Natta M, Behling C, Contos MJ, Cummings OW, et al. Design and validation of a histological scoring system for nonalcoholic fatty liver disease. Hepatology 2005;41(6):1313-21.         [ Links ]

21. Li L, Zhang L, Pan S, Wu X, Yin X. No significant association between vitamin D and nonalcoholic fatty liver disease in a Chinese population. Digestive diseases and sciences 2013;58(8):2376-82.         [ Links ]

22. Katz K, Brar PC, Parekh N, Liu YH, Weitzman M. Suspected nonalcoholic Fatty liver disease is not associated with vitamin d status in adolescents after adjustment for obesity. Journal of obesity 2010;2010:496829.         [ Links ]

23. Roth CL, Elfers CT, Figlewicz DP, Melhorn SJ, Morton GJ, Hoofnagle A, et al. Vitamin D deficiency in obese rats exacerbates nonalcoholic fatty liver disease and increases hepatic resistin and Toll-like receptor activation. Hepatology 2012;55(4):1103-11.         [ Links ]

24. Nakano T, Cheng YF, Lai CY, Hsu LW, Chang YC, Deng JY, et al. Impact of artificial sunlight therapy on the progress of non-alcoholic fatty liver disease in rats. J Hepatol 2011;55(2):415-25.         [ Links ]

25. Sharifi N, Amani R, Hajiani E, Cheraghian B. Does vitamin D improve liver enzymes, oxidative stress, and inflammatory biomarkers in adults with non-alcoholic fatty liver disease? A randomized clinical trial. Endocrine 2014.         [ Links ]

26. Aller R, Castrillon JL, de Luis DA, Conde R, Izaola O, Sagrado MG, et al. Relation of osteocalcin with insulin resistance and histopathological changes of non alcoholic fatty liver disease. Annals of hepatology 2011;10(1):50-5.         [ Links ]

27. Pietschmann P, Resch H, Muller C, Woloszczuk W, Willvonseder R. Decreased serum osteocalcin levels in patients with liver cirrhosis. Bone and mineral 1990;8(2):103-8.         [ Links ]

28. Lee NK, Sowa H, Hinoi E, Ferron M, Ahn JD, Confavreux C, et al. Endocrine regulation of energy metabolism by the skeleton. Cell 2007;130(3):456-69.         [ Links ]

29. Reis JP, von Muhlen D, Kritz-Silverstein D, Wingard DL, Barrett-Connor E. Vitamin D, parathyroid hormone levels, and the prevalence of metabolic syndrome in community-dwelling older adults. Diabetes Care 2007;30(6):1549-55.         [ Links ]

30. Chiu KC, Chuang LM, Lee NP, Ryu JM, McGullam JL, Tsai GP, et al. Insulin sensitivity is inversely correlated with plasma intact parathyroid hormone level. Metabolism: clinical and experimental 2000;49(11):1501-5.         [ Links ]

31. Lee DM, Rutter MK, O'Neill TW, Boonen S, Vanderschueren D, Bouillon R, et al. Vitamin D, parathyroid hormone and the metabolic syndrome in middle-aged and older European men. European journal of endocrinology / European Federation of Endocrine Societies. 2009;161(6):947-54.         [ Links ]

32. Kayaniyil S, Vieth R, Harris SB, Retnakaran R, Knight JA, Gerstein HC, et al. Association of 25(OH)D and PTH with metabolic syndrome and its traditional and nontraditional components. The Journal of clinical endocrinology and metabolism 2011;96(1):168-75.         [ Links ]

33. Minambres I, de Leiva A, Perez A. Hypovitaminosis D and metabolic syndrome. Medicina clinica 2014.         [ Links ]

34. Moreiro J, Ruiz O, Perez G, Salinas R, Urgeles JR, Riesco M, et al. Parathyroid hormone and bone marker levels in patients with morbid obesity before and after biliopancreatic diversion. Obesity surgery 2007;17(3):348-54.         [ Links ]

35. Alvarez V, Cuevas A, Olivos C, Berry M, Farias MM. Micro-nutrient deficiencies one year after sleeve gastrectomy. Nutricion hospitalaria 2014;29(1):73-9.         [ Links ]



Rubén Díez-Rodríguez.
Digestive Disease Department.
Complejo Asistencial Universitario de León.
Altos de Nava S/N.
24008. León. Spain.

Recibido: 14-VIII-2014.
Aceptado: 18-IX-2014.