“Vitamin D: Link between Osteoporosis, Obesity and Diabetes”

Vitamin D refers to a steroid hormone performing many physiologicalroles. It is linked to osteoporosis, obesity and diabetes due to itsfunctions in prevention or treatment. Vitamin D enhances calcium andphosphorous plasma levels, controls osteoblast, and deals with thehypersecretion of PTH (parathyroid hormone), during bone metabolism.As a result, the hormone helps in forming bones as well as avoidingor curing osteoporosis. Concerning obesity and diabetes, vitamin Drestrains the collection of fat, improves insulin production, andreduces resistance to insulin, in addition to minimizing hunger thatmay result in overeating.

Link to Osteoporosis

Vitamin D raises the phosphorous as well as calcium plasma levelsduring bone metabolism, important during mineralization (Candido &ampBressan, 2014). It is important that calcium circulate to ensurecorrect performance of nerve diffusion, hormone production andneuromuscular junctions, in PTH. The functions improve the density ofbone mineral in turn minimizing the peril of reducing throughenhancing muscle tone, in turn decreasing osteoporosis as well as itsaftermaths. When in an active state, Vitamin D has the ability toboost calcium as well as phosphorous levels, which are normallycirculating (Candido &amp Bressan, 2014). The boosting restoresnormal levels via pathways.

First is triggering the intake of levels in intestines, specificallyjejunum and duodenum. This happens because of calcium pathways thatopen. Vitamin D improves the intestine intake level of calcium thatis 10-15% when in passive transportation, 30-40% during normalsituations and increases to 60-80% when expectant and lactating(Candido &amp Bressan, 2014). Second, is the pathway that happensvia bone mobilization of phosphorous, as well as calcium. Theprocedure is characterized by an enhanced expression of receptorsthat trigger ligand proteins within osteoblasts, able to hold topre-osteoclast RANK in turn supporting the resorption of bone(Candido &amp Bressan, 2014). The osteoblasts have vitamin D thattriggers the production of proteins linked to the shaping of bones.These are osteocalcin and controlled production of osteopontin.Vitamin D has an express role in osteoclasts via triggeringosteoclastogenesis, though the undeviating role through osteoblastsbecomes more apparent (Candido &amp Bressan, 2014). Third, is apathway that relies on PTH and entails the rise in renal calciumretaining because of enhanced tubular re-uptake or a drop of filteredload (Candido &amp Bressan, 2014).

Mineralization regards to a passive procedure that merely happens inthe presence of ample amounts of calcium and vitamin D (Candido &ampBressan, 2014). A shortage of vitamin D means a drop in calciumcirculation or a rise in PTH. PTH enhances hydroxylase kidney actionthat eventually improves the serum amount of vitamin D, a powerfulmechanism during bone resorption. During the phase, flowing vitamin Dlevels as well as calcium become standard, compromising bone reserves(Candido &amp Bressan, 2014). A prolonged lack of vitamin D resultsin reduced substrates that are necessary in synthesizing vitamin D inits active state. The loss of bone results in osteoporosis. Contrary,when there is a normal supply of vitamin D, there are ample levels ofcalcium circulation in the blood (Candido &amp Bressan, 2014).Notably, bone loss happens due to unevenness, with enhancedresorption concerning formation. Vitamin D enhances the forming ofbones through enhancing intestine calcium intake, as well as dealingwith hypersecretion of PTH.

Link to Obesity

Research depicts that persons having obesity often have anabnormally low circulating vitamin D. Two views explain the link amidvitamin D and obesity. One, obesity could result in reduced “serum25-hydroxyvitamin D concentrations” or it could be probable thatreduced circulation of the hormone might result in obesity or hinderlosing weight (Earthman et al, 2012). A number of possible mechanismsexplain how obesity leads to low “serum 25-hydroxyvitamin D”.When adipose tissue results in vitamin D sequestration, the outcomeis decreased vitamin D in persons that have obesity. There seems tobe more intake and holding of vitamin D that is fat-soluble, throughadipose tissue when compared to persons with normal body weight.

A number of hypotheses explain how obesity leads to low vitamin D. Arise in vitamin D catabolism because of enhancing adiposity arisingfrom the 24-hydroxylase activity apparent in adipose tissue is one ofthe hypotheses (Luong &amp Nguyen, 2013). A different inferencenotes that vitamin D production through the liver could happen at areduced level in obese persons compared to those without obesity(Earthman et al, 2012). Obesity is linked to “non-alcoholic fattyliver” illness, while research notes that persons having theillness had low “serum 25-hydroxyvitamin D” levels. Further isthe argument that obesity arises from lack of exposure to sunlight,resulting in insufficiency, possibly due to minimal engagement inoutdoor work and dressing in manners that minimally expose the skinto sunlight (Earthman et al, 2012).

When vitamin D is low, it could impede weight loss. In vitroresearch has assessed the impacts PTH as well as vitamin D has onadipose tissue to demonstrate how vitamin D results in anti-obesity(Seppa, 2013). The conclusion has been that, depending on theconcentration level, vitamin D seems to impede the differentiation ofadipose tissue via compressing lipoprotein lipase. In a differentstudy linked to vitamin D’s possibility in restricting adiposity,“fatty acid synthase” gene expression, a significant enzymeengaged in adipose lipogenesis appeared restrained by high vitamin Dlevels (Jung &amp Mok, 2014). This demonstrates a possibleanti-obesity activity by vitamin D, causing obese individuals not toloss excess weight.

Link to Diabetes

There is a link amid vitamin D and both type 1 and 2 diabetes (NIH,2013). Type 1 arises from the immune systems malfunction. Amplescientific proof demonstrates that vitamin D has a crucial functionin ensuring normal immune system functioning. Deficiency may resultin malfunctioning. Lifestyles attributed to type 2 diabetes involveaging, lack of exercise and obesity, which are factors that as wellresult in reducing vitamin D in the body (Scragg, 2008). Vitamin D iseffective in ensuring normal glucose metabolism through acting oncells that make insulin within the pancreas, triggering them toproduce more. The hormone acts on fat as well as muscle cells withthe objective of enhancing insulin activity through minimizinginsulin resistance. It decreases inflammation that is apparent inindividuals that have type 2 diabetes. In addition, vitamin D has anindirect function of increasing the making of insulin and itsactivity through enhancing calcium levels within the cells.


Candido, F. G &amp Bressan, J. (2014). Vitamin D: link betweenosteoporosis, obesity and diabetes. International Journal ofMolecular Sciences, 15 (4), 6569-6591.

Earthman, C. P., Beckman, L. M., Masodkar, K &amp Sibley, S. D.(2012). The link between obesity and low circulating25-hydroxyvitamin D concentrations: considerations and implications.International Journal of Obesity, 36, 387-396.

Jung, C. H &amp Mok, J. (2014). Vitamin D and obesity. The KoreanJournal of Obesity, 23 (4), 236-241.

Luong, K &amp Nguyen, L. (2013). The beneficial role of vitamin D inobesity: possible genetic and cell signaling mechanisms. Journal, 12, 89.

NIH, National Institutes of Health. (2013). Large study toexamine if vitamin D prevents diabetes, 1-1. Retrieved from:

Scragg, R. (2008). Vitamin D and Type 2 Diabetes. AmericanDiabetes Association, 57(10), 2565-2566.

Seppa, N. (2013). Link between obesity and vitamin D clarifies.Science News, 1-1. Retrieved from: