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Does Vitamin D Decide Whether Calories Become Fat Or Muscle? Mechanisms Of Caloric Partitioning In Metabolic Health

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dr Karunia Valeriani Japar

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Introduction

Vitamin D deficiency is highly prevalent worldwide and has traditionally been conceptualized primarily as a disorder of skeletal health, classically associated with rickets, osteomalacia, and osteoporosis. However, accumulating evidence over the past two decades has repositioned vitamin D as a pleiotropic endocrine hormone, with its receptor and metabolizing enzymes identified in multiple extra-skeletal tissues, including skeletal muscle, adipose tissue, pancreatic b-cells, and immune cells. This broadened tissue distribution suggests that vitamin D may play an integral role in systemic energy homeostasis and substrate utilization, extending far beyond calcium-phosphate balance.

Within this expanded biological framework, a key emerging question is whether vitamin D status can influence “caloric partitioning” that is, the allocation of ingested energy toward adipose storage versus lean tissue accretion. Preclinical studies indicate that high-dose vitamin D can divert surplus calories away from white adipose depots and toward skeletal muscle mass and linear growth, implying a hormone-sensitive bias in nutrient destiny under conditions of energy surplus. Complementing these findings, observational human data consistently link low circulating 25-hydroxyvitamin d concentrations with higher overall adiposity, greater intramuscular fat accumulation, and increased insulin resistance, although causality remains incompletely defined.

Against this background, the present review examines vitamin d as a potential modulator of caloric partitioning across the lifespan, integrating mechanistic insights from vitamin D receptor biology with data from animal models and human studies of body composition and metabolic health. Particular emphasis is placed on aging and the prevention of metabolic disease, including obesity, insulin resistance, and sarcopenic obesity, conditions in which dysregulated nutrient allocation is central to pathophysiology. Finally, the review explores how these insights may be operationalized within digital and AI-enabled health platforms, where integration of vitamin D status into predictive models and personalized interventions could support more favourable distribution of calories toward metabolically protective lan tissue and away from ectopic and visceral fat stores.

Vitamin D Biology Beyond Bone

Vitamin D circulates predominantly as 25-hydroxyvitamin D [25(OH)D], which is sequentially hydroxylated to active hormone 1,25-dihydroxyvitamin d [1,25(OH)2D] that exerts its biological actions through the vitamin D receptor (VDR), a nuclear receptor regulating the transcription of a wide array of target genes. Beyond classical calcium-phosphate homeostasis, VDR and vitamin D metabolizing enzymes are expressed in multiple extra-skeletal tissues, including adipose tissue, skeletal muscle, pancreatic b-cells, liver, and diverse immune cell subsets, positioning vitamin D as a systemic modulator of energy and glucose metabolism [1,2,3,4,5].

Figure 1. Dietary Vitamin D Absorption Activation Process [3]

Experimental models have shown that VDR signalling directly influences mitochondrial function, fatty acid b-oxidation, and the expression of uncoupling proteins (UCPs), processes that are central to energy expenditure and substrate utilization. In VDR-null mice, higher rates of adipose tissue b-oxidation, upregulation of UCP1-3, and increased oxygen consumption collectively indicate a shift toward greater basal energy expenditure and resistance to fat accumulation. Within skeletal muscle, vitamin D signalling affects calcium handling, contractile performance, and fiber phenotype, and lack of VDR has been linked to altered mitochondrial protein regulation and a shift toward a more oxidative muscle profile under metabolic stress [4,6,7,8,9].

At the level of the pancreatic islet, both VDR and the 1-a-hydroxylase enzyme are expressed in b-cells, enabling local conversion of 25(OH)D to 1,25(OH)2D and autocrine regulation of gene transcription. In vitro and in vivo studies indicate that active vitamin D can modulate insulin gene expression, enhance glucose-stimulated secretion, and protect b-cells from inflammatory and oxidative injury, thereby linking vitamin d signalling to b-cell survival and insulin secretory capacity. Through the integrated actions of VDR in adipose tissue, skeletal muscle and b-cells, vitamin D emerges as an important endocrine factor in the orchestration of whole-body energy balance, substrate partitioning, and glucose homeostasis [1,2,3,4,6,10,11,12].

Evidence That Vitamin D Affects Body Composition

Observational data from cross-sectional and longitudinal cohorts consistently demonstrate an inverse association between serum 25-hydroxyvitamin d [25(OH)D] concentrations and indices of adiposity, including body mass index (BMI), total fat mass, and central adiposity across children, adults, and older population. In several studies, individuals with vitamin D insufficiency exhibit greater intramuscular fat infiltration and less favourable lean-to-fat ratios even at comparable levels of overall adiposity, suggesting that low 25(OH)D may be linked not only to the quantity but also to the distribution and ectopic deposition of fat. Recent dose-response analyses further indicate that adults with higher fat mass require substantially larger vitamin D doses to achieve and maintain target 25(OH)D levels, consistent with sequestration of vitamin D in adipose tissue and/or altered metabolism in states of obesity. Collectively, these findings support a potentially bidirectional relationship in which excess adiposity lowers bioavailable vitamin D, while chronic vitamin D deficiency may contribute to an adiposity-promoting milieu [2,13,14,15,16,17].

Figure 2. The role of oxidative stress in bone disorders and the protective role of vitamin D [16]

Interventional and experimental data provide additional support for a role of vitamin D signalling in body composition, while also highlighting important species and context differences. In a recent mouse model exposed to caloric surplus, high-dose dietary vitamin D promoted greater gains in lean mass and linear growth while limiting fat accumulation, effectively reallocating excess energy away from adipose tissue toward muscle and skeletal growth. Earlier work in VDR-null mice showed reduced adipose mass, smaller adipocytes, increased fatty acid b-oxidation, and upregulation of uncoupling proteins, along with elevated energy expenditure and relative resistance to diet-induced obesity, underscoring the importance of VDR signalling in adipose tissue and whole-body energy metabolism [6,7,18].

Figure 3. Visual abstract: high dose dietary vitamin D preferentially allocates excess calories to muscle and growth instead of fat by increasing leptin production and sensitivity and decreasing myostatin production [18]

By contrast, human supplementation trials have yielded more modest and heterogeneous effects on body composition, with outcomes strongly influenced by baseline vitamin D status, degree of adiposity, dose, and concomitant lifestyle factors. Some randomized and non-randomized studies in deficient, obese, or high-risk populations report small but favourable changes, including reductions in visceral or hepatic fat, improvements in lean mass indices, or better preservation of muscle function, whereas other trials show minimal or no effect on weight or fat mass despite robust increases in 25(OH)D. Taken together, experimental evidence supports a biologically plausible role for vitamin D and VDR signalling in the regulation of body composition and caloric partitioning, but in humans the magnitude and consistency of these effects appear context dependent, likely interacting with diet composition, physical activity, and the presence of obesity or metabolic disease [19,20,21,22].

Mechanistic Pathways: From Vitamin D To Caloric Partitioning

Insulin Sensitivity And Glucose Handling

Vitamin D exerts direct effects on insulin biology through several complementary molecular pathways. Pancreatic b-cells express both the vitamin D (VDR)  and the 1-a-hydroxylase enzyme, enabling local conversion of 25-hydroxyvitamin D to the active hormone and autocrine regulation of insulin gene transcription. The insulin gene promoter contains functional vitamin D response elements that can be activated by 1,25-dihydroxyvitamin D, thereby influencing insulin synthesis at the transcriptional level. Beyond transcriptional control, vitamin D modulates intracellular and extracellular calcium handling b-cells, which is critical for glucose-stimulated insulin exocytosis, and it protects b-cells from inflammatory cytokine and oxidative stress-induced apoptosis , preserving endocrine capacity under metabolic stress [1,4,10,11,12,13].

In skeletal muscle, vitamin d signalling enhances insulin sensitivity through multiple mechanisms. Experimental studies demonstrate that active vitamin D can upregulate insulin receptor expression and improve post-receptor insulin signalling, facilitating greater glucose uptake and glycogen storage in muscle fibers while reducing ectopic lipid accumulation. By augmenting muscle insulin action, vitamin D may shift postprandial nutrient flux away from de novo lipogenesis in adipose tissue and toward glycogen repletion and protein anabolism in muscle, a pattern consistent with favourable caloric partitioning. Clinical investigations across adult and pediatric populations have reported inverse associations between serum 25(OH)D concentrations and indices of insulin resistance, such as HOMA-IR, although the magnitude of effects varies by age, adiposity, and baseline vitamin D status [2,4,14,16].

Randomized intervention trials have yielded mixed results, with some studies showing modest improvements in insulin sensitivity and glucose tolerance following vitamin D supplementation, particularly in deficient or insulin-resistant individuals, while others report minimal metabolic benefit. These heterogeneous outcomes likely reflect differences in dose, duration, and the presence of confounding lifestyle factors such as diet and physical activity. Nonetheless, the mechanistic evidence from b-cells and muscle studies supports a model in which adequate vitamin d status enhances insulin action, reduces chronic hyperinsulinemia, and promotes allocation of glucose and amino acids toward muscle anabolism rather than adipose lipogenesis, thereby contributing to healthier body composition and metabolic resilience [2,4,10,12,14,16].

Adipose Tissue And VDR Signalling

Adipose tissue is now recognized as a key extra-skeletal target of vitamin D signalling. Adipocytes express the vitamin D receptor (VDR) as well as the enzymes required for local activation and inactivation of vitamin d metabolites, enabling tissue-specific regulation of gene programs involved in lipogenesis, lipolysis, thermogenesis and adipokine secretion. In vivo studies indicate that 1,25-dihydroxyvitamin D can modulate triglyceride storage and breakdown by influencing pathways of fatty acid uptake, synthesis, and mobilization, and can alter the expression of hormones such as leptin and adiponectin that communicate adipose energy status to other organs. These findings position adipose tissue not only as a storage depot for vitamin D but also as an active site where vitamin D-VDR signalling shapes local and systemic energy metabolism [6,18,23,24,25,26].

Genetic models manipulating VDR expression in adipose tissue provide compelling mechanistic evidence that vitamin D signalling contributes to the “thriftiness” or “wasting” of excess calories. global VDR-null mice display a lean phenotype with reduced fat mass, smaller white adipocytes, lower plasma triglycerides and leptin, and marked upregulation of uncoupling proteins (UCP1-3) and fatty acid b-oxidation in white and brown adipose depots, changes that are accompanied by increased oxygen consumption and resistance to diet-induced obesity these data suggest that loss of VDR activity drives a more energy-expending state in adipose tissue, favouring dissipation of surplus energy as heat rather than storage as triglyceride. Conversely, transgenic overexpression of human VDR specifically in adipocytes results in increased fat mass and obesity despite unchanged food intake, associated with reduced energy expenditure, lower fatty acid b-oxidation and lipolysis, and suppression of thermogenic and lipid-handling genes in white and brown adipose tissue. Together, these reciprocal models support a paradigm in which vitamin D, VDR signalling within adipose tissue helps set the energetic tone of the organism, promoting a more energy-conserving, fat-storing phenotype when VDR signalling is high, and a more energy-wasting, fat-resistant phenotype when VDR activity is absent or reduced, thereby influencing whether excess calories are ultimately stored as triglycerides or dissipated via thermogenesis [6,7,18,23,24,26].

Skeletal Muscle, Mitochondrial Function, And Lean Mass

Skeletal muscle is a major extra-skeletal target of vitamin D and a dominant determinant of whole-body energy expenditure, given its large contribution to resting and activity-related oxygen consumption. Both the vitamin d receptor (VDR), and CYP27B1, the enzyme that converts 25-hydroxyvitamin D to its active form, are expressed in myofibers and satellite cells, enabling local activation of vitamin D, VDR signalling regulates the expression of hundreds of nuclear genes involved in mitochondrial biogenesis, respiratory electron transport, and contractile function, indicating a coordinated role in maintaining oxidative metabolism and muscle integrity [27,28,29,30,31,32,33].

Figure 4. Overview of biological functions of vitamin D with the emphasis on skeletal muscle [27]

Mechanistically, loss of VDR function in skeletal muscle, either through global deficiency or muscle-specific VDR knockout, reduces mitochondrial respiration, ATP production from oxidative phosphorylation, and the content or activity of key electron transport chain complexes, leading to impaired mitochondrial oxidative capacity and lower whole-body energy expenditure. Conversely, exposure of muscle cells to 1,25‑dihydroxyvitamin D enhances mitochondrial oxygen consumption, improves coupling of respiration to ATP synthesis, upregulates genes controlling mitochondrial fusion and biogenesis, and attenuates reactive oxygen species production and proteolytic pathways, thereby supporting a more oxidative, fatigue‑resistant phenotype. In parallel, vitamin D modulates myogenesis by inhibiting excessive myoblast proliferation, promoting differentiation and myotube formation, and increasing the expression of myogenic regulatory factors, while VDR overexpression in vivo stimulates skeletal muscle hypertrophy through enhanced anabolic signalling, ribosomal biogenesis, and muscle protein synthesis [28,29,30,31,32,33].

The mitochondrial and anabolic actions have direct implications for caloric partitioning. By improving mitochondrial oxidative capacity and ATP generation in skeletal muscle, adequate vitamin D status facilitates greater oxidation of fatty acids and glucose within muscle fibers, decreasing reliance on adipose tissue for energy storage and limiting ectopic lipid accumulation. Simultaneously, vitamin D driven support of muscle regeneration, fiber size, and strength increases total lean mass, thereby expanding the body’s metabolically active compartment and elevating resting energy expenditure. Human data, though heterogeneous, are directionally consistent: in older vitamin D deficient individuals, supplementation has been associated with improvements in muscle mass, strength, and mitochondrial function, alongside shifts in body composition suggestive of reduced fat and preserved or increased lean tissue. Taken together, these findings support a model in which vitamin d, via VDR signalling in skeletal muscle, enhances oxidative metabolism and anabolic capacity, biasing surplus calories toward muscle maintenance and function rather than long-term storage in adipose depots [28,29,30,31,32,34,35].

Aging, Metabolic Disease, And Clinical Implications

Across the lifespan, low vitamin D status tends to cluster with key components of the metabolic aging phenotype, including obesity, insulin resistance, type 2 diabetes, and progressive loss of skeletal muscle mass and function. Epidemiological studies in diverse populations show that individuals with lower circulating 25‑hydroxyvitamin D [25(OH)D] concentrations have higher prevalence of metabolic syndrome, insulin resistance, and type 2 diabetes, even after partial adjustment for adiposity and lifestyle factors, suggesting that hypovitaminosis D may act both as a marker and a potential modifier of cardiometabolic risk. In older adults, vitamin D deficiency is also consistently associated with reduced muscle strength and physical performance, higher rates of frailty, and greater incidence of adverse outcomes such as falls, fractures, disability, and mortality. When low vitamin D status coexists with reduced lean mass and increased fat mass, sarcopenic obesity, cross‑sectional and longitudinal data indicate a particularly adverse phenotype characterized by heightened risks of insulin resistance, metabolic syndrome, cardiovascular disease, and functional decline [14,15,16,36,37,38,39,40,41,42,43,44].

Mechanistic and interventional work supports a contributory role of vitamin D within this metabolic aging framework. Experimental studies link vitamin D deficiency to impaired insulin secretion, reduced insulin sensitivity in skeletal muscle and adipose tissue, and low‑grade inflammation, all of which promote ectopic lipid accumulation and glucolipotoxicity over time. In parallel, vitamin D–VDR signalling in skeletal muscle influences mitochondrial function, muscle protein turnover, and regenerative capacity, thereby affecting the trajectory of sarcopenia and sarcopenic obesity in later life. Clinical trials and meta‑analyses, although heterogeneous, suggest that correcting vitamin D deficiency may modestly improve muscle strength, physical performance, and the response to resistance training, particularly when combined with adequate protein (e.g. whey or leucine‑rich formulations) in older, high‑risk adults. These findings are consistent with a model in which maintaining sufficient vitamin D status supports more favourable caloric partitioning, directing nutrients toward preservation of lean mass and oxidative capacity rather than disproportionate storage as visceral and ectopic fat, as individuals age [16,28,29,36,39,42,45,46,47].

From a preventive medicine perspective, vitamin D should be viewed as one component of an integrated strategy for healthy metabolic aging rather than a stand‑alone solution. Optimizing 25(OH)D levels in line with current guidelines, when combined with resistance training, sufficient high‑quality protein intake (approximately 1.2–1.6 g/kg/day in older adults), and broader lifestyle optimization (sleep, physical activity, and dietary pattern), may help mitigate the development of sarcopenic obesity and related metabolic disorders. For AI‑enabled metabolic health programs, incorporating vitamin D data, either via laboratory 25(OH)D measurement or proxy variables such as adiposity, outdoor activity, and dietary pattern into risk prediction models and personalization engines offers a practical opportunity. Digital platforms integrating vitamin D status with continuous cardiometabolic signals (e.g. glycemia, activity, body composition) could stratify users by risk of sarcopenia, sarcopenic obesity, and type 2 diabetes, and then tailor interventions such as resistance‑training prescriptions, protein and micronutrient targets, and follow‑up intervals to preserve muscle, limit ectopic fat, and enhance metabolic resilience with aging [36,44,45,46,47,48,49].

Limitations And Research Gaps

The current evidence base linking vitamin D to body composition and caloric partitioning is constrained by several important methodological and translational limitations. Most human data are derived from cross‑sectional or longitudinal observational studies, in which lower 25‑hydroxyvitamin D [25(OH)D] is consistently associated with higher adiposity, insulin resistance, and adverse metabolic profiles, but these designs cannot reliably disentangle cause from consequence. Obesity itself alters vitamin D kinetics through volumetric dilution, sequestration in adipose tissue, and changes in hepatic and renal metabolism, making reverse causation and residual confounding difficult to exclude. In addition, many cohorts lack precise phenotyping of ectopic fat depots and muscle quality (e.g. MRI or CT for visceral and intramuscular fat), limiting the ability to link vitamin D status to finer‑grained patterns of caloric partitioning [14,15,16,17,42,43,44].

Interventional studies are similarly heterogeneous. Randomized controlled trials vary widely in vitamin D dose, formulation, baseline 25(OH)D status, treatment duration, and the selection of primary endpoints, with many designed around bone or glycemic outcomes rather than body composition or caloric partitioning per se. Few trials rigorously standardize or co‑prescribe key lifestyle co‑interventions such as resistance training, protein intake, or weight‑loss strategies, and relatively few use high‑resolution methods (DXA, MRI, spectroscopy) to assess changes in regional adiposity, intramuscular fat, or organ‑specific ectopic lipid. These design features contribute to mixed and often small effect sizes in meta‑analyses, and make it difficult to define dose–response relationships, optimal target ranges, or thresholds beyond which additional vitamin D confers little body‑composition benefit [14,16,39,42,45,46,47].

Preclinical studies, while mechanistically informative, raise their own translational challenges. Mouse models employing supraphysiologic vitamin D dosing, global VDR knockout, or tissue‑specific VDR overexpression demonstrate robust effects on adiposity, mitochondrial function, and energy expenditure, but the relevance of these extreme perturbations to typical human deficiency or supplementation ranges is uncertain. Species differences in vitamin D metabolism, diet composition, thermogenic regulation, and muscle–adipose cross‑talk further complicate direct extrapolation from rodents to humans [6,7,18,24,50,51].

Consequently, several research gaps remain. First, there is a need for well‑powered, long‑duration randomized trials that enroll carefully characterized subgroups, such as individuals who are frankly deficient, obese, insulin resistant, or older with sarcopenic obesity and that combine vitamin D optimization with standardized resistance training, protein intake, and, where relevant pharmacotherapy (e.g. GLP‑1 receptor agonists). These studies should incorporate high‑resolution imaging of visceral, hepatic, and intramuscular fat, along with functional outcomes (strength, VO2 max, insulin sensitivity) to directly test whether improved vitamin D status shifts caloric partitioning toward lean mass and away from ectopic fat. Second, integrative approaches using digital and AI‑enabled health platforms could help identify phenotypes most responsive to vitamin D–centered interventions, by continuously linking 25(OH)D levels with granular data on diet, activity, sleep, glycemia, and body composition over time. Addressing these gaps will be essential to clarify whether vitamin D is primarily a marker, a modest modifier, or a meaningful lever for improving caloric partitioning and metabolic resilience in clinical practice [28,29,36,39,42,44,45,46,47,48,49].

Conclusion

Vitamin D has emerged as more than a skeletal hormone; it functions as a metabolic regulator with the potential to influence how surplus energy is partitioned between adipose storage and the accretion or preservation of lean tissue. Preclinical models and mechanistic work demonstrate that vitamin D and vitamin D receptor (VDR) signalling in skeletal muscle, adipose tissue, and pancreatic b-cells modulate pathways governing energy expenditure, mitochondrial function, insulin secretion and sensitivity, and tissue-specific substrate use, collectively supporting a role in caloric partitioning at organ and whole-body level.

In humans, low circulating 25-hydroxyvitamin D is consistently associated with higher overall and central adiposity, greater intramuscular fat, and increased insulin resistance, while intervention studies in deficient or high-risk populations suggest that vitamin D repletion can produce modest improvements in body composition, muscle function, and select metabolic parameters, albeit with heterogeneous and context-dependent effect sizes. Taken together, these data support the view that optimizing vitamin D status is a plausible, though not standalone, lever to favour more metabolically advantageous caloric partitioning when combined with established interventions such as targeted nutrition, resistance training, sleep optimization, and where appropriate, pharmacotherapy. For clinicians and AI-driven health-tech platforms focused on aging and metabolic disease prevention, incorporating vitamin D into risk stratification and personalized care pathways is reasonable, provided that current uncertainties regarding causality, magnitude of benefit, and ideal therapeutic windows are acknowledged and addressed through ongoing, rigorously designed translational research.

References

  1. Dragovic T, Slavica Radjen, Branka Djurovic, Rabrenovic V. Extraskeletal activity of vitamin D and a potential association with diabetes mellitus. Vojnosanitetski pregled. 2016 May 25;74(5):476–82.
  2. Kalra S, Goyal R. Vitamin D deficiency: a cause of clinical concern. International Journal of Research in Medical Sciences. 2025 Apr 18;
  3. Park CY, Han SN. The Role of Vitamin D in Adipose Tissue Biology: Adipocyte Differentiation, Energy Metabolism, and Inflammation. Journal of Lipid and Atherosclerosis [Internet]. 2021 May 1;10(2):130–44. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8159757/
  4. Argano C, Mirarchi L, Amodeo S, Orlando V, Torres A, Corrao S. The role of vitamin D and its molecular bases in insulin resistance, diabetes, metabolic syndrome, and cardiovascular disease: State of the art. International Journal of Molecular Sciences. 2023 Oct 23;24(20):15485–5.
  5. Bikle D. Vitamin D: Production, Metabolism, and Mechanisms of Action [Internet]. Nih.gov. MDText.com, Inc.; 2021. Available from: https://www.ncbi.nlm.nih.gov/books/NBK278935/
  6. Wong KE, Szeto FL, Zhang W, Ye H, Kong J, Zhang Z, et al. Involvement of the vitamin D receptor in energy metabolism: regulation of uncoupling proteins. American Journal of Physiology-Endocrinology and Metabolism. 2009 Apr;296(4):E820–8.
  7. Su H, Lou Y, Fu Y, Zhang Y, Liu N, Liu Z, et al. Involvement of the Vitamin D Receptor in Energy Metabolism Revealed by Profiling of Lysine Succinylome of White Adipose Tissue. Scientific Reports. 2017 Oct 26;7(1).
  8. Das A, Neha Jawla, Meena V, Gopinath SD, Gopalakrishnan Aneeshkumar Arimbasseri. Lack of vitamin D signalling shifts skeletal muscles towards oxidative metabolism. Journal of Cachexia Sarcopenia and Muscle. 2023 Dec 2;15(1):67–80.
  9. Zienab Alrefaie, Awad H, Khadeejah Alsolami, Hamed EA. Uncoupling proteins: are they involved in vitamin D3 protective effect against high-fat diet-induced cardiac apoptosis in rats? Archives of Physiology and Biochemistry. 2019 Dec 3;128(2):438–46.
  10. Bornstedt ME, Gjerlaugsen N, Pepaj M, Bredahl MKL, Thorsby PM. Vitamin D Increases Glucose Stimulated Insulin Secretion from Insulin Producing Beta Cells (INS1E). International Journal of Endocrinology and Metabolism. 2019 Jan 7;In Press(In Press).
  11. Lee S, Clark SA, Gill RK, Christakos S. 1,25-Dihydroxyvitamin D3 and pancreatic beta-cell function: vitamin D receptors, gene expression, and insulin secretion. Endocrinology. 1994 Apr;134(4):1602–10.
  12. Mohd Ghozali N, Giribabu N, Salleh N. Mechanisms Linking Vitamin D Deficiency to Impaired Metabolism: An Overview. Xie Z, editor. International Journal of Endocrinology. 2022 Jul 6;2022:1–16.
  13. He LP, Li CP, Liu CW, Gu W. The Regulatory Effect of Vitamin D on Pancreatic Beta Cell Secretion in Patients with Type 2 Diabetes. Current Medicinal Chemistry. 2024 Aug 7;31.
  14. Deng Y, Luo Y, Shen Y, Zhao Y, Cao W, Cao J, et al. Associations between hypovitaminosis D, adiposity indices and insulin resistance in adolescents: mediation analyses from NHANES 2011–2018. Nutrition & Diabetes. 2025 Feb 4;15(1).
  15. Dai D, Ling Y, Xu F, Li H, Wang R, Gu Y, et al. Impact of body composition on vitamin D requirements in healthy adults with vitamin D deficiency. Frontiers in Endocrinology. 2025 Jul 3;16.
  16. Abed MN, Alassaf FA, Qazzaz ME. Exploring the Interplay between Vitamin D, Insulin Resistance, Obesity and Skeletal Health. Journal of Bone Metabolism. 2024 May 31;31(2):75–89.
  17. Tobias DK, Luttmann-Gibson H, Mora S, Danik J, Bubes V, Copeland T, et al. Association of Body Weight With Response to Vitamin D Supplementation and Metabolism. JAMA Network Open [Internet]. 2023 Jan 17;6(1):e2250681. Available from: https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2800490
  18. Xu Y, Lou Y, Kong J. VDR regulates energy metabolism by modulating remodeling in adipose tissue. European Journal of Pharmacology. 2019 Dec;865:172761.
  19. Chou SH, Murata EM, Yu C, Danik J, Kotler G, Cook NR, et al. Effects of Vitamin D3 Supplementation on Body Composition in the VITamin D and OmegA-3 TriaL (VITAL). The Journal of Clinical Endocrinology & Metabolism. 2021 Feb 1;106(5):1377–88.
  20. Medeiros JFP, de Oliveira Borges MV, Soares AA, dos Santos JC, de Oliveira ABB, da Costa CHB, et al. The impact of vitamin D supplementation on VDR gene expression and body composition in monozygotic twins: randomized controlled trial. Scientific Reports. 2020 Jul 20;10(1).
  21. Oussaada SM, Akkermans I, Chohan S, Limpens J, Twisk JWR, Winkler C, et al. The effect of active vitamin D supplementation on body weight and composition: A meta-analysis of individual participant data. Clinical Nutrition. 2024 Nov;43(11):99–105.
  22. Musazadeh V, Zarezadeh M, Ghalichi F, Kalajahi FH, Ghoreishi Z. Vitamin D supplementation positively affects anthropometric indices: Evidence obtained from an umbrella meta-analysis. Frontiers in Nutrition. 2022 Sep 7;9.
  23. Abbas MA. Physiological functions of Vitamin D in adipose tissue. The Journal of Steroid Biochemistry and Molecular Biology. 2017 Jan;165:369–81
  24. Mutt SJ, Hyppönen E, Saarnio J, Järvelin MR, Herzig KH. Vitamin D and adipose tissue—more than storage. Frontiers in Physiology [Internet]. 2014 Jun 24;5. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4067728/
  25. Hewison M, Bouillon R, Giovannucci E, Goltzman D, Meyer M, Welsh J. Feldman and Pike’s Vitamin D. Academic Press; 2023.
  26. Cimini FA, Federica Sentinelli, Oldani A, Ilaria Barchetta, Cavallo MG. Adipose Tissue Dysfunction and Metabolic Diseases: The Role of Vitamin D/Vitamin D Receptor Axis. International Journal of Molecular Sciences. 2025 Oct 22;26(21):10256–6.
  27. Dzik KP, Kaczor JJ. Mechanisms of vitamin D on skeletal muscle function: oxidative stress, energy metabolism and anabolic state. European Journal of Applied Physiology [Internet]. 2019 Mar 4;119(4):825–39. Available from: https://link.springer.com/article/10.1007%2Fs00421-019-04104-x
  28. Salles J, Chanet A, Guillet C, Anouk MM. Vaes, Brouwer-Brolsma EM, Rocher C, et al. Vitamin D status modulates mitochondrial oxidative capacities in skeletal muscle: role in sarcopenia. 2022 Nov 24;5(1).
  29. Girgis CM, Brennan‐Speranza TC. Vitamin D and Skeletal Muscle: Current Concepts from Preclinical Studies. JBMR Plus. 2021 Oct 29;
  30. Latham CM, Brightwell CR, Keeble AR, Munson BD, Thomas NT, Zagzoog AM, et al. Vitamin D Promotes Skeletal Muscle Regeneration and Mitochondrial Health. Frontiers in Physiology. 2021 Apr 14;12.
  31. Alavala Matta Reddy, Iqbal M, Chopra H, Shaheda Urmi, Sunil Junapudi, Bibi S, et al. Pivotal role of vitamin D in mitochondrial health, cardiac function, and human reproduction. PubMed. 2022 Jan 1;21:967–90.
  32. Vernerová L, Vokurková M, Laiferová NA, Nemec M, Špiritović M, Mytiai O, et al. Vitamin D and its receptor in skeletal muscle are associated with muscle disease manifestation, lipid metabolism and physical fitness of patients with myositis. Arthritis Research & Therapy. 2025 Mar 4;27(1).
  33. Srikuea R, Hirunsai M, Charoenphandhu N. Regulation of vitamin D system in skeletal muscle and resident myogenic stem cell during development, maturation, and ageing. Scientific Reports. 2020 May 19;10(1).
  34. Kirwan R, Isanejad M, Davies IG, Mazidi M. Genetically Determined Serum 25-Hydroxyvitamin D Is Associated with Total, Trunk, and Arm Fat-Free Mass: A Mendelian Randomization Study. The Journal of nutrition, health and aging. 2022 Jan;26(1):46–51.
  35. Bass JJ, Nakhuda A, Deane CS, Brook MS, Wilkinson DJ, Phillips BE, et al. Overexpression of the vitamin D receptor (VDR) induces skeletal muscle hypertrophy. Molecular Metabolism. 2020 Dec;42:101059.
  36. Zhang F, Li W. Vitamin D and Sarcopenia in the Senior People: A Review of Mechanisms and Comprehensive Prevention and Treatment Strategies. Therapeutics and Clinical Risk Management. 2024 Sep 1;Volume 20:577–95.
  37. Batsis JA, Villareal DT. Sarcopenic obesity in older adults: aetiology, epidemiology and treatment strategies. Nature Reviews Endocrinology. 2018 Jul 31;14(9):513–37.
  38. Alvarez-Mejia M, Restrepo CA, Marulanda-Mejia F, González-Correa CH. Association between hypovitaminosis D and sarcopenic obesity in patients with chronic kidney disease stages 3 and 4. Clinical Nutrition ESPEN. 2025 Feb;65:205–8.
  39. Kelishadi R, Salek S, Salek M, Hashemipour M, Movahedian M. Effects of vitamin D supplementation on insulin resistance and cardiometabolic risk factors in children with metabolic syndrome: a triple-masked controlled trial. Jornal de Pediatria. 2014 Jan;90(1):28–34.
  40. Mi W, Zhang H, Zhang L, Li X, Wang Z, Sun Y, et al. Age but not vitamin D is related to sarcopenia in vitamin D sufficient male elderly in rural China. Scientific Reports [Internet]. 2025 Jan 4 [cited 2025 Sep 20];15(1). Available from: https://www.nature.com/articles/s41598-025-85468-3?fromPaywallRec=false
  41. Roh E, Choi KM. Health Consequences of Sarcopenic Obesity: A Narrative Review. Frontiers in Endocrinology. 2020 May 21;11.
  42. Sung CC, Liao MT, Lu KC, Wu CC. Role of Vitamin D in Insulin Resistance. Journal of Biomedicine and Biotechnology. 2012;2012:1–11.
  43. Buchmann N, Eckstein N, Spira D, Demuth I, Steinhagen‐Thiessen E, Norman K. Vitamin D insufficiency is associated with metabolic syndrome independent of insulin resistance and obesity in young adults ‐ The Berlin Aging Study II. Diabetes/Metabolism Research and Reviews. 2021 Apr 30;37(8).
  44. Wu W, Zhou JC, Yang L. Surveillance and Evaluation of Vitamin D Nutrition and its Health Impact in Chinese Older Adults. The Journal of Nutrition. 2025 Jan;
  45. Carrillo AE, Flynn MG, Pinkston C, Markofski MM, Jiang Y, Donkin SS, et al. Impact of vitamin D supplementation during a resistance training intervention on body composition, muscle function, and glucose tolerance in overweight and obese adults. Clinical Nutrition. 2013 Jun;32(3):375–81.
  46. Agergaard J, Trøstrup J, Uth J, Iversen JV, Boesen A, Andersen JL, et al. Does vitamin-D intake during resistance training improve the skeletal muscle hypertrophic and strength response in young and elderly men? – a randomized controlled trial. Nutrition & Metabolism. 2015 Sep 30;12(1).
  47. Nasrin Nasimi, Sohrabi Z, Nunes EA, Sadeghi E, Jamshidi S, Gholami Z, et al. Whey Protein Supplementation with or without Vitamin D on Sarcopenia-Related Measures: A Systematic Review and Meta-Analysis. Advances in Nutrition. 2023 Jul 1;14(4):762–73.
  48. Theodore Armand TP, Kim HC, Kim JI. Digital Anti-Aging Healthcare: An Overview of the Applications of Digital Technologies in Diet Management. Journal of Personalized Medicine [Internet]. 2024 Mar 1;14(3):254. Available from: https://www.mdpi.com/2075-4426/14/3/254
  49. Huynh P, Fleisch E, Brändle M, Kowatsch T, Jovanova M. Digital health technologies for metabolic disorders in older adults: a scoping review protocol. BMJ Open. 2024 Dec;14(12):e085797.
  50. Roizen J, Long C, Casella A, Nguyen M, Danahy L, Seiler C, et al. High dose dietary vitamin D allocates surplus calories to muscle and growth instead of fat via modulation of myostatin and leptin signaling. Research square [Internet]. 2024 Aug;rs.3.rs4202165. Available from: https://pubmed.ncbi.nlm.nih.gov/38766160/
  51. Wong KE, Kong J, Zhang W, Szeto FL, Ye H, Deb DK, et al. Targeted Expression of Human Vitamin D Receptor in Adipocytes Decreases Energy Expenditure and Induces Obesity in Mice. Journal of Biological Chemistry. 2011 Aug 12;286(39):33804–10.

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