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November/December 2025

CPE Monthly: Vitamin D in Diabetes

Katie Chapmon, MS, RD28 Mins Read

Today’s Dietitian
Vol. 27 No. 9 P. 34

Take this course and earn 2 CEUs on our Continuing Education Learning Library

Suboptimal vitamin D status can potentially affect the development of diabetes. The function of vitamin D can be seen in the overall process of insulin secretion and beta cell function. The accumulating evidence suggests that altered vitamin D and calcium homeostasis may play direct and indirect roles in the development of this disease state.

This continuing education course reviews the metabolism of vitamin D, the interrelationship between vitamin D and diabetes, and the mechanisms of this relationship to diabetes and its complications.

Function of Vitamin D

Vitamin D is a unique element—it acts as both a vitamin and hormone and plays a central role in a variety of metabolic pathways. Vitamin D is considered a fat-soluble vitamin available in the forms ergocalciferol (D2) and cholecalciferol (D3). Because there are few foods that naturally contain adequate sources of vitamin D, some foods are fortified with the vitamin.1,2 Cholecalciferol is the naturally occurring form and is synthesized in the skin after exposure to sunlight, whereas ergocalciferol is typically used as a food additive and in prescription doses of vitamin D.

The biological function of vitamin D is to regulate and normalize circulating blood levels of calcium and phosphorus. Vitamin D also helps in bone formation and maintenance, as it assists with calcium absorption. The kidneys create the biologically active form of vitamin D. Many immune cells, such as the epithelia of the skin, gut, prostate, lung, bone, parathyroid gland, and pancreatic islets contain the machinery for the two-step conversion process to this active form. These local immune cells control the functioning of the vitamin D and utilize it as a hormone both as an intracrine factor to regulate intracellular events and as a paracrine factor to affect the gland and immune cells surrounding it. Receptors are present in these selected target organs and tissues, and vitamin D serves as a chemical messenger to transmit signals and rapid responses, such as the opening of ion channels.3,4

Vitamin D Metabolism

After vitamin D is either ingested or converted in the skin due to sunlight, it enters circulation and is transported to the liver and kidneys. Vitamin D is hydroxylated twice to biologically activate and become a secosteroid, in the following manner3,4:

• Vitamin D is first transported to the liver, where it’s converted to 25-hydroxyvitamin D, or 25(OH)D. Vitamin D is then bound to a carrier protein called the vitamin D binding protein and transported through circulation.

• Serum 25(OH)D3, the main circulating form, is typically used as the reliable indicator of vitamin D status in the body.

• In the kidneys, the second hydroxylation occurs: An enzyme called CYP27B1 hydroxylase changes it into the biologically active form 1,25-dihydroxyvitamin D3, or 1,25(OH)2D3.

Although the kidneys are the main source in finalizing this process, other cells are able to perform this multistep metabolism, as mentioned above.

The 1,25(OH)2D3 plays a central role in a variety of metabolic pathways in the body.3,4

Vitamin D Deficiency

According to the Endocrine Society, 18% to 41% of people in the United States have vitamin D insufficiency while 3% to 32% have a deficiency of vitamin D. The Endocrine Society considers insufficiency as a 25(OH)D concentration between 21 and 29 ng/mL and deficiency as ≤20 ng/mL for 25(OH)D concentration.5 The National Health and Nutrition Examination Survey (NHANES) data from 2001 to 2018 reported 2.6% having severe deficiency, 22% moderate deficiency, and 40.9% insufficiency. They defined insufficiency as 25(OH)D concentrations between 50 and 75 ng/mL, and moderate deficiency as 25 to 50 ng/mL, while a 25(OH) D concentration <25 ng/mL is considered severely deficient.6

Clinical manifestations of vitamin D deficiency vary depending on the severity. In children, it’s characterized by bowed legs and is commonly referred to as rickets. Bowed legs are caused by the disruption of bone mineralization and widening of the epiphyseal plates of the long bones. Other symptoms in children include growth retardation and “rachitic rosary,” a widening of the anterior ribs at the costochondral junction.1

In adults, the clinical manifestations are different because the deficiency occurs after skeletal maturation and fusing of the epiphyseal plates. Although a low vitamin D level may not produce symptoms, it can cause adverse effects. Adults with progressing deficiencies in the moderate-to-severe level may experience muscle weakness, bone pain, and difficulty walking. Vitamin D deficiency can lead to loss of bone, increase fracture risk, and contribute to osteoporosis, osteomalacia, and osteopenia.1,2

Research linking low vitamin D to diabetes, CVD, cancer, infection, and autoimmune diseases continues to be an area of focus. Vitamin D assists in increased cell differentiation and limits proliferation, as uncontrolled proliferation of cell mutations during this process can potentially lead to cancer. Deficiency in vitamin D may also affect immune function by upsetting the immune response environment and potentially leading to autoimmune dysfunction.7

Factors Contributing to Low Vitamin D Levels

There are several environmental, genetic, and cultural influences on vitamin D status. Sunlight can potentially provide someone with their vitamin D requirements. Lack of sun exposure due to concealing clothing, sun safety measures, skin pigmentation, or geographic location, including latitude, altitude, and atmosphere, contribute to the inability for ultraviolet radiation to penetrate and stimulate the skin epidermis to synthesize vitamin D.7 According to a 2011 article by Balk, application of sunscreen with a sun-protection factor as low as 10 can reduce the availability and production of vitamin D by 90%.2,8

Naturally occurring vitamin D is limited, and most foods containing vitamin D are fortified. Because there’s a high degree of variability in the content of vitamin D in fortified foods, vitamin D requirements generally can’t be achieved through food. Vitamin D insufficiency or deficiency are also related to the inability of absorption through the digestive tract or decreased kidney functionality to convert vitamin D into an active form. Persons with diabetes may be at significant risk with added renal impairment, nerve dysfunction affecting the digestive tract, and, possibly, genetic predisposition.1,2

Genetic Predisposition to Diabetes

Type 1 diabetes etiology is characterized by destruction of the insulin-producing beta cells in the pancreas islets of Langerhans by the body’s immune system. Due to this origin, it’s classified as an autoimmune disorder. On the other hand, type 2 diabetes is a chronic metabolic disease with its main characteristics being insulin resistance and inadequate insulin production by the beta cell. The severity of insulin resistance in clinical presentation depends on the intensity of failing beta cell function.3

Certain variants of the human leukocyte antigen class II genes, part of the human leukocyte antigen complex family, increase the risk of developing type 1 diabetes. This complex helps the immune system react appropriately by distinguishing between proteins made by the body and those made by harmful invaders. Certain variations of these genes increase the risk of inappropriate immune response to pancreatic beta cells. These variations occur in the general population; approximately 40% of those possessing these certain variations continue in the development of type 1 diabetes.9

According to the National Institutes of Health, 150 DNA variations have been associated with the risk of developing type 2 diabetes. The genetic variations affect expression of the gene in development and function of beta cells, release and processing of insulin, and insulin sensitivity. Gene expression can include the change in amount, timing, and location of gene activity. These variations, combined with health and lifestyle factors, are likely to influence the risk of developing type 2 diabetes.10

As previously mentioned, the vitamin D endocrine system provides biological functions, such as cell growth and cell differentiation.11 Vitamin D receptors are present in different tissues, including the pancreatic beta cells and almost every cell of the immune system. They provide physiological effects such as calcium transport and cell growth and differentiation. The various genes that encode the vitamin D receptors can create different genotype combinations. The vitamin D receptor has demonstrated an indirect effect on the disease process.

Inflammatory cytokines and interferon production signals macrophages and cytotoxic T cells in the pancreas. The progressive destruction of pancreatic islet cells at the early stages of type 1 diabetes is the outcome of the inability to activate macrophages and cytotoxic T cells. Vitamin D inhibits the production of these signaling proteins, therefore reducing stress and eventual apoptosis.11,12

The presence of the vitamin D receptor on the beta cells contained in the pancreatic islets may affect the ability of the islets to produce active 25(OH)D. The increased intercellular calcium in the islet due to the lack of vitamin D receptor conversion can additionally restrict the beta cell insulin. Similar to how genetic predisposition may affect diabetes onset, there are conflicting data on the correlation between the various vitamin D receptor polymorphisms and genetic development of diabetes.1-4

The role of vitamin D in maintaining normal glucose metabolism is reflected in the presence of the vitamin D receptor in the insulin-responsive tissues and the pancreatic beta cells. In addition, insulin regulation is assisted by the presence of the vitamin D receptor, the expression of CYP27B1 hydroxylase, and the presence of a vitamin D response element in the human insulin receptor gene promoter.

CYP27B1 hydroxylase is the enzyme involved in the second of the two reactions to create the active form of vitamin D. The bioactive form, 1,25(OH)2D3, performs several processes in insulin regulation: activating human insulin receptor gene transcription, stimulating insulin receptors, and assisting in insulin-mediated glucose transport. 1,25(OH)2D3 also directly modulates the generation and effects of inflammatory cytokines to reduce systemic inflammation and, consequently, insulin resistance.3,13

Cojic et al studied the effects of high dose (14,000 IU) daily oral vitamin D supplementation on subjects who have diabetes that were both deficient and nondeficient in vitamin D. In both groups there were improvements in HgbA1c over six months. For those that were deficient, prescription dose of vitamin D (50,000 IU) followed by the daily high dose supplementation demonstrated a significant decrease in advanced oxidation protein product levels over the initial three month period.14

Pattern of Vitamin D Immune Regulation and Progression to Type 1 Diabetes in Genetically Predisposed Individuals

The hypothesis of the connection between type 1 diabetes and vitamin D status comes from epidemiologic observation of those with higher incidence of vitamin D deficiency and increased risk of developing autoimmune diseases. The active form of vitamin D is involved in the homeostasis in the immune system, and the function of vitamin D is thought to be connected.3

Vanherwegen and colleagues found that patients with type 1 diabetes had a higher prevalence of vitamin D deficiency, based on a meta-analysis of several observational studies.3 However, there are conflicting data on the immune regulation response from vitamin D and the progression to type 1 diabetes. In two studies comparing people newly diagnosed with type 1 diabetes with age- and sex-matched participants without diabetes, low levels of circulating vitamin D were seen in participants with diabetes.15 A 2014 prospective study by Raab and colleagues followed a cohort of children with type 1 diabetes and measured vitamin D status and progression of diabetes over five or 10 years. There was no correlation found between vitamin D and the development of type 1 diabetes.16

Vitamin D and Insulin Sensitivity

In an analysis of data from the National Health and Nutrition Examination Survey, serum 25(OH)D was inversely correlated with type 2 diabetes incidence and insulin resistance. Vitamin D deficiency is also linked to insulin sensitivity, including resistance and secretion.3

Insulin secretion is influenced by a calcium flux through the cell membrane, creating a calcium-dependent process. Calbindin is a calcium-binding protein regulated by vitamin D. This protein, which modulates insulin release, is found primarily in the beta cells. By regulating intracellular calcium and utilizing depolarization to stimulate insulin release, calbindin irregularity affects insulin secretion. The parathyroid hormone (PTH) is another mechanism that affects insulin secretion and synthesis and promotes insulin resistance. Elevated PTH inhibits synthesis and beta cell secretion and, in target cells, promotes resistance. Vitamin D deficiency affects calbindin and can induce secondary hyperparathyroidism.11

Peripheral insulin resistance has a similar relationship to vitamin D. Surrounding tissues such as adipose tissues and skeletal muscle can initiate an insulin response that utilizes a small amount of calcium. These insulin-mediated intracellular processes use vitamin D to stimulate the expression of insulin receptors. Vitamin D also regulates the calcium flux within these tissues. The change in the intracellular calcium can impair signal pathways, decreasing glucose transport. The decreased glucose transportation pathway may also play a role in peripheral insulin resistance.11

A final consideration of the relationship between vitamin D and insulin resistance involves the renin-angiotensin-aldosterone system. In this pathway, renin is needed to synthesize angiotensin II. Vitamin D deficiency suppresses renin formation, which indirectly affects the creation of angiotensin II. In vascular and skeletal muscle tissue, angiotensin II inhibits insulin action, therefore impairing glucose uptake. In this scenario, vitamin D could regulate the renin-angiotensin-aldosterone system.11

Vitamin D and Beta Cell Function

Impaired beta cell function and insulin resistance are seen in the development of type 2 diabetes. Vitamin D directly affects the beta cell functioning in glucose regulation. The vitamin D receptor expressed in the beta cells and the binding of 1,25(OH)2D to that receptor by the enzyme CYP27B1 hydroxylase is a commonly occurring process in the beta cells. By changing the vitamin into an active form, it influences the insulin gene promoter and the activation of the human insulin gene.

In addition, vitamin D itself increases beta cell resistance to apoptosis and increases beta cell replication. Vitamin D is essential to the entire process of beta cell functioning and insulin regulation. Without vitamin D, impaired functioning and regulation of the insulin process can occur.11,12 In a 2022 study from Derosa et al, the restoration of vitamin D in those with type 2 diabetes led to an improvement of glycemic control, but also reduced use of some oral hypoglycemic agents and some types of insulin used.17

Vitamin D and Diabetes Complications

Diabetes increases the risk of other health complications when blood glucose is elevated. Vitamin D can also play a part in the relationship between diabetes and these health conditions.

Kidney

The kidneys, which contain receptors that turn vitamin D into its active form, are one of the critical areas in the vitamin D system. The relationship between diabetes and chronic kidney disease (CKD) can potentially further the development of vitamin D deficiency. Active vitamin D controls the absorption of calcium and phosphorus, which maintains mineral balance and PTH regulation. Compromised kidneys lessen the ability to activate vitamin D. In turn, vitamin D isn’t available to regulate calcium and phosphorus, resulting in an overactive PTH. As discussed previously, an elevated PTH inhibits synthesis and beta cell secretion and promotes insulin resistance.

An older, but important 2007 study of National Health and Nutrition Examination Survey III participants evaluated kidney function, insulin resistance, and serum 25(OH)D levels and confirmed significantly lower levels of serum 25(OH) D in those with comprised kidneys.18 Vitamin D is usually administered to those with kidney disease to suppress PTH production to keep the hormone at a functioning level.19 Recommendations from the Kidney Disease Outcomes Quality Initiative include initiating vitamin D supplementation in those with CKD stages 2 to 4 with a serum 25(OH) >30 ng/mL and elevated PTH and for CKD 5, initiating vitamin D supplementation in those with PTH >300 pg/mL regardless of serum 25(OH) status.20

CVD

A study by Stančáková Yaluri et al found that vitamin D deficiency was the strongest factor associated with all-cause mortality through a 5.6 year study in patients with type 2 diabetes at high cardiovascular risk. Researchers found that a reduction of 10 ng/mL was associated with a two-fold increase in all-cause mortality.21 Similarly, in those with prediabetes and intermediate CVD risk, regardless of vitamin D status, demonstrated small improvements in atherosclerotic CVD risk score.22

According to the American Heart Association, diabetes is one of the seven major controllable risk factors for CVD.23 The positive association between hypertension and insulin resistance increases the risk of CVD. Vitamin D can lower blood pressure due to its role in the renin-angiotensinaldosterone system. Renin is an enzyme that catalyzes the splitting of a small peptide from a larger protein. This small peptide, angiotensin I, cleaves into angiotensin II.

Angiotensin II is another peptide that can increase the constriction of small arteries and retention of sodium and water, thereby influencing blood pressure. 1,25(OH)2D interacts with the vitamin D receptor and reduces the gene that encodes renin. Renin controls the rate at which angiotensin II is created. It’s hypothesized that with less renin and, in turn, less angiotensin II created, it’s less likely that blood pressure would be influenced. Intervention studies have reviewed the possibility of vitamin D supplementation to prevent or regulate hypertension in this system, but there are no conclusive results at this time.7

Those with diabetes often have high LDL cholesterol, low HDL cholesterol, and high triglycerides. This lipid triad characterizes diabetic dyslipidemia, a lipid disorder associated with insulin resistance. A 2014 meta-analysis of 17 trials in those with type 2 diabetes found that vitamin D supplementation improved all three lipid measurements in diabetic dyslipidemia.24

However, a 2019 study by Angellotti and colleagues looking at the effect of daily 4,000-IU vitamin D supplementation on lipid profile and cardiovascular risk among patients with stable type 2 diabetes suggested otherwise. When compared with a placebo, vitamin D supplementation didn’t improve lipid profile and cardiovascular risk in those with stable type 2 diabetes without vitamin D deficiency. Surprisingly, favorable trends were observed among those in this cohort who weren’t taking cholesterol medication.25

Cancer

Diabetes and cancer share similar risk factors, and although there isn’t an established direct correlation between the two disease states, there’s a higher incidence of certain cancers in those who have diabetes.26 The connection between cancer and vitamin D was first hypothesized after it was observed that those living in Northern latitudes who had increased vitamin D deficiency also had an increased risk of cancer. A large meta-analysis by Kuznia et al that included 14 randomized control trials of varied vitamin D doses and regimens, found a 12% reduction in cancer mortality in those given vitamin D compared with placebo.27

As more attention is paid to vitamin D and its connection with cancer, research is taking a closer look at the vitamin D receptor and its influence on active vitamin D in site-specific tissues for those cancers. Active vitamin D, upon connecting with the vitamin D receptor, can inhibit cell differentiation, proliferation, and apoptosis. This influence applies to both cancerous and noncancerous cells. Current research focuses on colon and breast cancer and the relationship with vitamin D; however, there’s no conclusive evidence to confirm the connection.7

Nerve Functioning

Diabetic neuropathy is damage to nerve functioning experienced by those with diabetes. While some patients believe the only symptoms of neuropathy are tingling or numbness in the feet, it can also cause nerve dysfunction in internal organs. This condition is seen in those with high glucose levels and hyperlipidemia.

According to the National Institute of Diabetes and Digestive and Kidney Diseases, there are four main types of neuropathy that affect people with diabetes: peripheral, autonomic, focal, and proximal. Peripheral is the most common, affecting approximately one-third to one-half of those with diabetes. Nerve damage from this type is seen in the feet, legs, and hands. Autonomic neuropathy affects the nerve function of internal organs such as the digestive tract, heart rate, sweat glands, and eyes, and may affect blood. Focal neuropathy is site specific and seen as a type of entrapment condition, which causes direct compression on an individual nerve. The hands, head, and torso are the areas usually affected. Finally, proximal neuropathy, which is rare, affects a nerve in the hip, leg, or buttocks and can cause incapacitation that gradually improves over months or years, though it’s unlikely that symptoms will completely resolve.28

Diabetic neuropathy has been linked to vitamin D status. It’s uncertain whether vitamin D could be a therapeutic application for the development and pain associated with neuropathy, but it’s something to consider. A 2020 study looked at administering high-dose vitamin D supplementation to diabetic subjects with signs of peripheral neuropathy. The researchers found that 40,000 IU of vitamin D per week for 24 weeks resulted in a significant decrease in neuropathic severity and reduced inflammatory markers such as interleukin-6.29 In a 2022 review by Putz et al, researchers found that vitamin D deficiency plays a significant role in the development of several neuropathies and diabetic foot ulcers. They also found the use of vitamin D supplementation as an effective adjuvant therapy for neuropathic pain and reduced progression of neural damage.30

Bone Health

Vitamin D is vital to the integrity of bone mineralization, but there’s also a link between bone health and diabetes. Increased risk of fracture and poorer bone quality is seen in people with diabetes, especially type 1. The theory of this connection begins with type 1 diabetes onset occurring at a relatively young age, before a child’s bone reaches peak mass. Peak bone mass includes the strength and density of the bones, which don’t reach full development in individuals until they’re in their 20s.31

Vitamin D insufficiency is an integral factor in the development of osteoporosis, although the overall cause of a loss of bone density is often multifactorial. Insufficient vitamin D significantly reduces the uptake of calcium through the intestines. Decreased calcium leads to increased PTH secretion, thereby causing increased bone resorption. Prolonged elevation of the PTH results in osteoporosis, bone mineral density loss, and increased fracture risk.7

Fracture risk is more prevalent in those with poor blood sugar management, who have longstanding disease, and who use insulin. According to the National Institutes of Health, the risk of falls and fractures are increased due to complications from diabetes, such as nerve damage, muscle weakness, episodes of low blood sugar, and vision problems.31 Other factors contributing to fracture risk in addition to potential insufficient vitamin D intake must be taken into account.

Supplementation and Toxicity Risk

The nutritional vitamin D status is typically tested as serum 25(OH)D concentration. At this time, it seems to be the most reliable source of testing, though concentrations aren’t always reflected properly due to bioavailability, ethnicity, and body weight.7

It’s been difficult to find consensus concerning the standardization of vitamin D supplementation and testing. As with most recommendations, the overall health, age, body weight, outcome, nutrition, and cultural habits of an individual have to be taken into account. Therefore, overarching guidelines are difficult to set. Guidelines that are focused on bone health and osteoporosis prevention recommend serum 25(OH)D concentration of greater than 20 ng/mL and daily vitamin D doses between 400 and 800 IU based solely on age.

In contrast, the guidelines based on how vitamin D affects other medical conditions recommend serum 25(OH)D concentrations of 30 ng/mL or higher and doses between 400 and 2,000 IU daily, dependent on some of the individual factors mentioned previously.32 Supplementation is available in a variety of doses as a single ingredient or in combination with calcium.

Toxicity is rare in healthy adults with intakes of less than 10,000 IU vitamin D daily. Sun exposure hasn’t been seen to cause hypervitaminosis D. Elevated vitamin D can cause hypercalcemia, which promotes bone loss, kidney stones, and, with untreated levels over time, calcification of organs. Primary hyperparathyroidism, sarcoidosis, tuberculosis, and lymphoma can actually increase potential hypercalcemia in response to increased vitamin D intake and should be monitored by a medical team.7 The National Academy of Medicine has set the upper limit for vitamin D intake at 4,000 IU per day, a conservative amount compared with recommendation by other organizations.33,34

Putting It Into Practice

Vitamin D is functionally involved with insulin control in a transfer, receptor, or regulation capacity. Vitamin D can also affect numerous complications associated with diabetes. Due to its role in the development and complication of diabetes, tight monitoring of serum vitamin D and HgbA1c levels are recommended in those with or at high risk of developing diabetes. As HgbA1c levels increase, consideration of a vitamin D supplement should be reviewed.

Serum 25(OH)D testing is advised, with a concentration goal of 30 ng/mL or higher. Insufficient or deficient vitamin D levels should be treated to decrease the possibility of diabetes development. In those with a vitamin D deficiency, a referral to a prescribing physician may be needed for a prescription dose of ergocalciferol. Those with insufficient vitamin D should be advised to start daily supplementation of up to 4,000 IU per day. Once serum levels are normalized, ongoing supplementation of 1,000 to 2,000 IU per day should be recommended to ensure levels continue to stay within the normal range. Education surrounding the connection between vitamin D and diabetes, as well as the importance of continued supplementation, should be reviewed. Evaluation of vitamin D supplementation intake and consistency should be included in the treatment and monitoring of HgbA1c in patients with prediabetes or diabetes.

Unfortunately, vitamin D is difficult to obtain through food sources, even with fortified foods. Sun exposure can assist in vitamin D production through skin epidermis without sun protection.

At this point, it’s unclear whether vitamin D can be utilized as a complete therapeutic solution toward the prevention, progression, or outlying complications of diabetes. Further research will be needed to confirm the direct effects of vitamin D in this prevalent disease state.

— Katie Chapmon, MS, RD, is a Los Angeles–based private practice dietitian and consultant.

Learning Objectives

After completing this continuing education course, nutrition professionals should be better able to:

  1. Explain the significance between vitamin D status and potential progression of diabetes.
  2. Identify the interaction of vitamin D on insulin sensitivity and beta cell function.
  3. Apply information to current treatment and monitoring of diabetes.

Examination

1. How many times does vitamin D need to be hydroxylated in order to become biologically active?

  1. One
  2. Two
  3. Three
  4. Four

2. Which enzyme in the kidney is utilized in the second hydroxylation to create 1,25-dihydroxyvitamin D3 [1,25(OH)2D3]?

  1. BYT24Y7
  2. DOV67N8
  3. CYP27B1
  4. MQG92W4

3. What’s the name of the calcium-binding protein regulated by vitamin D?

  1. Insulin
  2. Cytokine
  3. Leukocyte
  4. Calbindin

4. Approximately what percentage of those possessing certain genetic variations go on to develop type 1 diabetes?

  1. 17%
  2. 36%
  3. 40%
  4. 50%

5. How does 1,25(OH)2D3 relate to type 2 diabetes?

  1. It reduces inflammatory cytokine effects and generation.
  2. It increases production of insulin in the pancreatic beta cells.
  3. It reduces cell reproduction.
  4. It increases turnover of the vitamin D receptor.

6. How does vitamin D deficiency affect renin?

  1. It increases renin formation.
  2. It suppresses renin formation.
  3. It increases renin’s glucose uptake.
  4. It increases renin’s creation of angiotensin.

7. Vitamin D directly affects beta cell functioning by which of the following?

  1. Increasing beta cell resistance to apoptosis
  2. Decreasing beta cell replication
  3. Decreasing vitamin D receptor access
  4. Increasing the availability of a specific enzyme

8. Toxicity is rare in those taking vitamin D supplements of less than what amount daily?

  1. 8,000 IU
  2. 10,000 IU
  3. 12,000 IU
  4. 20,000 IU

9. In the progression toward type 1 diabetes, vitamin D inhibits production of which signaling proteins?

  1. Macrophages and cytotoxic T cells
  2. Cytokines and interferon
  3. Leukocytes and beta cells
  4. Pepsin and trypsin

10. Vitamin D controls the absorption of which two minerals?

  1. Calcium and iron
  2. Calcium and magnesium
  3. Calcium and sodium
  4. Calcium and phosphorus

References

1. Penckofer S, Kouba J, Wallis DE, Emanuele MA. Vitamin D and diabetes: let the sunshine in. Diabetes Educ. 2008;34(6):939-940.

2. Vitamin D. The Nutrition Source — Harvard T.H. Chan School of Public Health website. https://www.hsph.harvard.edu/nutritionsource/vitamin-d/. Updated March 2023. Accessed January 14, 2024.

3. Vanherwegen AS, Gysemans C, Mathieu C. Vitamin D and diabetes. In: Feldman D, Pike JW, Bouillon R, Giovannucci E, Goltzman D, Hewison M, eds. Vitamin D. Volume 2: Health, Disease and Therapeutics. 4th ed. Cambridge, MA: Academic Press; 2017:969-987.

4. Grammatiki M, Rapti E, Karras S, Ajjan RA, Kotsa K. Vitamin D and diabetes mellitus: causal or casual association? Rev Endocr Metab Disord. 2017;18(2):227-241.

5. Endocrine Society. Endocrine facts and figures, first edition: bone and mineral. https://www.endocrine.org/-/media/endocrine/files/facts-and-figures/endocrine_facts_figures_bone_and_mineral.pdf. Published 2015. Accessed December 24, 2023.

6. Cui A, Xiao P, Ma Y, et al. Prevalence, trend, and predictor analyses of vitamin D deficiency in the US population, 2001–2018. Front Nutr. 2022;9:965376.

7. Vitamin D. Oregon State University, Linus Pauling Institute, Micronutrient Information Center website. https://lpi.oregonstate.edu/mic/vitamins/vitamin-D. Updated February 11, 2021. Accessed December 24, 2023.

8. Balk SJ. Council on Environmental Health; Section on Dermatology. Ultraviolet radiation: a hazard to children and adolescents. Pediatrics. 2011;127(3):e791-e817.

9. Type 1 diabetes. National Library of Medicine Genetics Home Reference website. https://ghr.nlm.nih.gov/condition/type-1-diabetes. Updated March 1, 2013. Accessed December 24, 2023.

10. Type 2 diabetes. National Library of Medicine Genetics Home Reference website. https://ghr.nlm.nih.gov/condition/type-2-diabetes. Updated November 1, 2017. Accessed December 24, 2023.

11. Harinarayan CV. Vitamin D and diabetes mellitus. Hormones (Athens). 2014;13(2):163-181.

12. Khan Z, Muhammad SA, Carpio J, et al. The effect of vitamin D supplementation on incidence of type 2 diabetes: a systematic review. Cureus. 2023;15(3):e36775.

13. Gu JC, Wu YG, Huang WG, et al. Effect of vitamin D on oxidative stress and serum inflammatory factors in the patients with type 2 diabetes. J Clin Lab Anal. 2022;36(5):e24430.

14. Cojic M, Kocic R, Klisic A, Kocic G. The effects of vitamin D supplementation on metabolic and oxidative stress markers in patients with type 2 diabetes: a 6-month follow up randomized controlled study. Front Endocrinol (Lausanne). 2021;12:610893.

15. Yu J, Sharma P, Girgis CM, Gunton JE. Vitamin D and beta cells in type 1 diabetes: a systematic review. Int J Mol Sci. 2022;23(22):14434.

16. Raab J, Giannopoulou EZ, Schneider S, et al. Prevalence of vitamin D deficiency in pre-type 1 diabetes and its association with disease progression. Diabetologia. 2014;57(5):902-908.

17. Derosa G, D’Angelo A, Martinotti C, et al. Vitamin D3 supplementation improves glycemic control in type 2 diabetic patients: results from an Italian clinical trial. Int J Vitam Nutr Res. 2022;92(2):91-100.

18. Chonchol M, Scragg R. 25-Hydroxyvitamin D, insulin resistance, and kidney function in the third National Health and Nutrition Examination Survey. Kidney Int. 2007;71(2):134-139.

19. Dorough H, Colman S. Vitamin D and chronic kidney disease. Davita Kidney Care website. https://www.davita.com/diet-nutrition/articles/basics/vitamin-d-and-chronic-kidney-disease. Accessed December 24, 2023.

20. Kramer H, Berns JS, Choi MJ, et al. 25-Hydroxyvitamin D testing and supplementation in CKD: an NKF-KDOQI controversies report. Am J Kidney Dis. 2014;64(4):499-509.

21. Stančáková Yaluri A, Tkáč I, Tokarčíková K, et al. Decreased 25-hydroxy vitamin D level is associated with all-cause mortality in patients with type 2 diabetes at high cardiovascular risk. Metabolites. 2023;13(8):887.

22. Desouza C, Chatterjee R, Vickery EM, et al. The effect of vitamin D supplementation on cardiovascular risk in patients with prediabetes: a secondary analysis of the D2d study. J Diabetes Complications. 2022;36(8):108230.

23. Cardiovascular disease and diabetes. American Heart Association website. https://www.heart.org/en/health-topics/diabetes/diabetes-complications-and-risks/cardiovascular-disease–diabetes. Updated May 4, 2021. Accessed December 24, 2023.

24. Messa P, Curreri M, Regalia A, Alfieri CM. Vitamin D and the cardiovascular system: an overview of the recent literature. Am J Cardiovasc Drugs. 2014;14(1):1-14.

25. Angellotti E, D’Alessio D, Dawson-Hughes B, et al. Effect of vitamin D supplementation on cardiovascular risk in type 2 diabetes. Clin Nutr. 2019;38(5):2449-2453.

26. Know the diabetes-cancer link. American Diabetes Association website. https://diabetes.org/about-diabetes/diabetes-prevention/diabetes-and-cancer. Accessed December 24, 2023.

27. Kuznia S, Zhu A, Akutsu T, et al. Efficacy of vitamin D3 supplementation on cancer mortality: systematic review and individual patient data meta-analysis of randomised controlled trials. Ageing Res Rev. 2023;87:101923.

28. Diabetic neuropathy. National Institute of Diabetes and Digestive and Kidney Diseases website. https://www.niddk.nih.gov/health-information/diabetes/overview/preventing-problems/nerve-damage-diabetic-neuropathies. Accessed December 24, 2023.

29. Karonova T, Stepanova A, Bystrova A, Jude EB. High-dose vitamin D supplementation improves microcirculation and reduces inflammation in diabetic neuropathy patients. Nutrients. 2020;12(9):2518.

30. Putz Z, Tordai D, Hajdú N, et al. Vitamin D in the prevention and treatment of diabetic neuropathy. Clin Ther. 2022;44(5):813-823.

31. What people with diabetes need to know about osteoporosis. NIH Osteoporosis and Related Bone Diseases National Resource Center website. https://www.bones.nih.gov/health-info/bone/osteoporosis/conditions-behaviors/diabetes. Updated May 2023. Accessed December 24, 2023.

32. Pludowski P, Holick MF, Grant WB, et al. Vitamin D supplementation guidelines. J Steroid Biochem Mol Biol. 2018;175:125-135.

33. Ross AC. The 2011 report on dietary reference intakes for calcium and vitamin D. Public Health Nutr. 2011;14(5):938-939.

34. Vieth R Holick MF. The IOM-Endocrine Society controversy on recommended vitamin D targets: in support of the Endocrine Society Position. In: Feldman D, Pike JW, Bouillon R, Giovannucci E, Goltzman D, Hewison M, eds. Vitamin D. Volume 1: Biochemistry, Physiology and Diagnostics. 4th ed. Cambridge, MA: Academic Press; 2017:1091-1107.

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