Research studies have linked vitamin D deficiency to diabetes, cancer, osteoporosis, and more. We’ve recently seen the importance of vitamin D even when it comes to COVID-19. Vitamin D has traditionally been known to play a role in calcium homeostasis and bone metabolism. Back in the 1900s, rickets became an epidemic that led to the fortification of milk with vitamin D, which still continues today. Now researchers from North Carolina (NC) State University have discovered a new link between vitamin D deficiency during early development and metabolic equilibrium in zebrafish.

The researchers published their findings,” Vitamin D deficiency serves as a precursor to stunted growth and central adiposity in zebrafish,” in the journal Scientific Reports.

The researchers observed groups of zebrafish between 2–12 months post-fertilization, and placed them on three engineered diets including a standard laboratory control diet, a vitamin D null diet, and a vitamin D enriched diet. The zebrafish spent four months on their particular diet, then the researchers focused on studying changes in their growth, bone density, triglyceride, lipid, cholesterol, and vitamin D levels. They discovered zebrafish in the vitamin D null diet were, on average, 50% smaller than those in the other two groups, and had significantly more fat reserves.

“While vitamin D has traditionally been associated with mineral ion homeostasis, accumulating evidence suggests non-calcemic roles for vitamin D including metabolic homeostasis. In this study, we examined the hypothesis that vitamin D deficiency (VDD) during early life stage development precedes metabolic disruption,” noted the researchers.

“The vitamin D deficient zebrafish exhibited both hypertrophy and hyperplasia—an increase in both the size and number of fat cells,” explained Seth Kullman, PhD, director of graduate programs and professor of toxicology at NC State. “They also had higher triglycerides and cholesterol, which are hallmarks of metabolic imbalance that can lead to cardio-metabolic disease. This, combined with the stunted growth, indicates that vitamin D plays an important role in the ability to channel energy into growth versus into fat storage.”

“Zebrafish grown on a vitamin D null diet between 2–12 months post-fertilization (mpf) exhibited diminished somatic growth and enhanced central adiposity associated with accumulation and enlargement of visceral and subcutaneous adipose depots indicative of both adipocyte hypertrophy and hyperplasia. VDD zebrafish exhibited elevated hepatic triglycerides, attenuated plasma free fatty acids, and attenuated lipoprotein lipase activity consistent with hallmarks of dyslipidemia,” wrote the researchers.

The vitamin D deficient zebrafish were given a vitamin D enriched diet for an additional six months, to see if the results could be reversed. The fish continued to grow and began to utilize fat reserves. However, they never caught up in size and retained residual fat deposits.

Stunted growth observed in the VDD zebrafish 6 mpf. (A) Both male and female VDD zebrafish exhibited stunted growth 6 mpf. Descending order: MALE (lab diet, VD3 sufficient, VDD), FEMALE (lab diet, VD3 sufficient, VDD). (B) Growth rate was taken biweekly starting at 2 mpf and ending at 6 mpf (2 mpf, 2.5 mpf, 3 mpf, etc.). At 6 mpf, the average SL (cm) for VDD, VD3 sufficient, and LD fish was 1.33 ± 0.0 cm, 2.21 ± 0.06 cm, and 2.25 ± -0.06 cm, respectively. Data are represented as mean ± SEM. (C) The SGR (%) from 2–6 mpf for VDD, VD3 sufficient, and LD fish was 1.72%, 2.69%, and 2.93%, respectively. Data are represented as mean ± SEM. All measures are representative of a mixed gender population. [Knuth, M.M., Mahapatra, D., Jima, D. et al. Vitamin D deficiency serves as a precursor to stunted growth and central adiposity in zebrafish. Sci Rep 10, 16032 (2020)]

“This work shows that vitamin D deficiency can influence metabolic health by disrupting the normal balance between growth and fat accumulation,” Kullman added. “Somehow the energy that should be going toward growth is getting shunted into creating fat and lipids, and this occurrence cannot be easily reversed. While we don’t yet understand the mechanism, we are beginning to tease that out.”

Moving forward, the researchers will focus on looking at the offspring of vitamin D deficient mothers, to determine whether this vitamin deficiency has epigenetic effects that can be passed down.

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