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TOPLINE:

The remission period of type 1 diabetes (T1D) can be prolonged with high-dose ergocalciferol (a vitamin D analog), by preserving the function of insulin-producing beta cells in newly diagnosed patients.

METHODOLOGY:

  • Beta cells may retain approximately 30%-50% function at the time of T1D diagnosis and continue producing insulin for months or years. Preserving beta-cell function early on can extend this remission period and improve long-term glycemic control.
  • Researchers conducted a secondary post hoc analysis of a randomized clinical trial looking at residual beta function and vitamin D supplementation in 36 youths (age, 10-21 years; mean age, 13.5 years; 33.3% women) with recently diagnosed T1D.
  • Participants were randomly assigned to receive vitamin D (50,000 international units) or placebo every week for 2 months and then biweekly for 10 months.
  • Mixed-meal tolerance tests were performed after overnight fasting at 0, 3, 6, 9, and 12 months, and blood draws were obtained 30 minutes and 90 minutes for post-meal C-peptide and glucose estimations.
  • The fasting proinsulin to C-peptide ratio (PI:C) and the percentage change in the area under the curve of C-peptide from baseline (%ΔAUC) were calculated to test the effect of vitamin D on beta-cell function.

TAKEAWAY: 

  • Vitamin D supplementation improved the insulin secretion capacity of beta cells, as observed by the decrease in the mean fasting PI:C ratio compared with placebo (−0.0009 vs 0.0011; P =.01).
  • The reduction in %ΔAUC of C-peptide was notably slower with vitamin D than placebo (−2.8% vs −4.7%; P =.03), indicating a longer delay in the loss of C-peptide.

IN PRACTICE:

“It is exciting to know that vitamin D could protect the beta cells of the pancreas and increase the natural production of good and functional insulin in these patients. This, in turn, prolongs the honeymoon phase of type 1 diabetes and leads to reduced long-term complications of this disease,” Benjamin Udoka Nwosu, MD, Northwell Health, Division of Endocrinology, Department of Pediatrics, Cohen Children’s Medical Center, New Hyde Park, New York, the principal author, said in a press release.

SOURCE:

The study was published online in JAMA Network Open.

LIMITATIONS:

It was a single-center study.

DISCLOSURES:

The study was supported by the National Institute of Diabetes and Digestive and Kidney Diseases. The authors did not report any conflicts of interest.

A version of this article appeared on Medscape.com.

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TOPLINE:

The remission period of type 1 diabetes (T1D) can be prolonged with high-dose ergocalciferol (a vitamin D analog), by preserving the function of insulin-producing beta cells in newly diagnosed patients.

METHODOLOGY:

  • Beta cells may retain approximately 30%-50% function at the time of T1D diagnosis and continue producing insulin for months or years. Preserving beta-cell function early on can extend this remission period and improve long-term glycemic control.
  • Researchers conducted a secondary post hoc analysis of a randomized clinical trial looking at residual beta function and vitamin D supplementation in 36 youths (age, 10-21 years; mean age, 13.5 years; 33.3% women) with recently diagnosed T1D.
  • Participants were randomly assigned to receive vitamin D (50,000 international units) or placebo every week for 2 months and then biweekly for 10 months.
  • Mixed-meal tolerance tests were performed after overnight fasting at 0, 3, 6, 9, and 12 months, and blood draws were obtained 30 minutes and 90 minutes for post-meal C-peptide and glucose estimations.
  • The fasting proinsulin to C-peptide ratio (PI:C) and the percentage change in the area under the curve of C-peptide from baseline (%ΔAUC) were calculated to test the effect of vitamin D on beta-cell function.

TAKEAWAY: 

  • Vitamin D supplementation improved the insulin secretion capacity of beta cells, as observed by the decrease in the mean fasting PI:C ratio compared with placebo (−0.0009 vs 0.0011; P =.01).
  • The reduction in %ΔAUC of C-peptide was notably slower with vitamin D than placebo (−2.8% vs −4.7%; P =.03), indicating a longer delay in the loss of C-peptide.

IN PRACTICE:

“It is exciting to know that vitamin D could protect the beta cells of the pancreas and increase the natural production of good and functional insulin in these patients. This, in turn, prolongs the honeymoon phase of type 1 diabetes and leads to reduced long-term complications of this disease,” Benjamin Udoka Nwosu, MD, Northwell Health, Division of Endocrinology, Department of Pediatrics, Cohen Children’s Medical Center, New Hyde Park, New York, the principal author, said in a press release.

SOURCE:

The study was published online in JAMA Network Open.

LIMITATIONS:

It was a single-center study.

DISCLOSURES:

The study was supported by the National Institute of Diabetes and Digestive and Kidney Diseases. The authors did not report any conflicts of interest.

A version of this article appeared on Medscape.com.

 

TOPLINE:

The remission period of type 1 diabetes (T1D) can be prolonged with high-dose ergocalciferol (a vitamin D analog), by preserving the function of insulin-producing beta cells in newly diagnosed patients.

METHODOLOGY:

  • Beta cells may retain approximately 30%-50% function at the time of T1D diagnosis and continue producing insulin for months or years. Preserving beta-cell function early on can extend this remission period and improve long-term glycemic control.
  • Researchers conducted a secondary post hoc analysis of a randomized clinical trial looking at residual beta function and vitamin D supplementation in 36 youths (age, 10-21 years; mean age, 13.5 years; 33.3% women) with recently diagnosed T1D.
  • Participants were randomly assigned to receive vitamin D (50,000 international units) or placebo every week for 2 months and then biweekly for 10 months.
  • Mixed-meal tolerance tests were performed after overnight fasting at 0, 3, 6, 9, and 12 months, and blood draws were obtained 30 minutes and 90 minutes for post-meal C-peptide and glucose estimations.
  • The fasting proinsulin to C-peptide ratio (PI:C) and the percentage change in the area under the curve of C-peptide from baseline (%ΔAUC) were calculated to test the effect of vitamin D on beta-cell function.

TAKEAWAY: 

  • Vitamin D supplementation improved the insulin secretion capacity of beta cells, as observed by the decrease in the mean fasting PI:C ratio compared with placebo (−0.0009 vs 0.0011; P =.01).
  • The reduction in %ΔAUC of C-peptide was notably slower with vitamin D than placebo (−2.8% vs −4.7%; P =.03), indicating a longer delay in the loss of C-peptide.

IN PRACTICE:

“It is exciting to know that vitamin D could protect the beta cells of the pancreas and increase the natural production of good and functional insulin in these patients. This, in turn, prolongs the honeymoon phase of type 1 diabetes and leads to reduced long-term complications of this disease,” Benjamin Udoka Nwosu, MD, Northwell Health, Division of Endocrinology, Department of Pediatrics, Cohen Children’s Medical Center, New Hyde Park, New York, the principal author, said in a press release.

SOURCE:

The study was published online in JAMA Network Open.

LIMITATIONS:

It was a single-center study.

DISCLOSURES:

The study was supported by the National Institute of Diabetes and Digestive and Kidney Diseases. The authors did not report any conflicts of interest.

A version of this article appeared on Medscape.com.

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