It turns out Bugs Bunny wasn’t just protecting his eyesight when he was munching on all those carrots. According to new research conducted at Lund University Diabetes Centre in Sweden, those same vitamin-A rich carrots could have been protecting him against diabetes too.
I’ll have more details on that new study in just a moment. But first let’s take a quick look at what we already knew about this often overlooked vitamin and diabetes.
Experts say vitamin A plays a role in the development of our beta-cells in early life when we’re still a fetus. But until very recently scientists had no idea that the vitamin may continue to play a role in those cells, or that not getting enough of it could be linked to diabetes.
Vitamin A deficiency linked to diabetes
Researchers at Weill Cornell Medical College in New York gave us our first solid hints of a possible connection. According to the Weill scientists vitamin A boosts beta cell activity, and lack of the vitamin could play a role in the development of type 2 diabetes.1
When the team genetically modified lab mice to be unable to store vitamin A their beta cells died, which means their bodies couldn’t produce insulin.
In a second experiment on a group of healthy mice the scientists removed all vitamin A from the critter’s diets. The mice lost a bunch of their beta cells, which led to drops in their insulin and rises in their blood sugar levels.
In other words they were well on their way to a type 2 diabetes diagnosis. But when they added A back into the rodent’s diets their bodies began producing more beta cells, insulin levels went back up and blood glucose dropped.
The researchers concluded that vitamin A deficiency was likely linked to type 2 diabetes. But more research was needed.
Which brings us to the new Lund University study published in the Endocrine Journal.2
Beta cells survive and thrive with A
The Swedish researchers discovered that insulin-producing beta cells have a bunch of receptors on their surfaces specifically designed for vitamin A. So they decided to find out more about the link between the vitamin and diabetes.
Working with insulin cells from mice and diabetic and non-diabetic donors they partially blocked the cell’s vitamin A receptors, and then introduced sugar.
The cell’s ability to secrete insulin dropped. And we’re not talking about a small dip either. Insulin secretion plummeted by close to 30 percent.
The lack of vitamin A also made the beta cells less resistant to inflammation. And cutting off the A completely killed the cells.
It’s now clear that vitamin A’s relationship to beta cells goes far beyond their development when we’re still in the womb. Vitamin A necessary for proper beta cell function throughout our lives.
Reduce your diabetes risk with vitamin A
In other words, the “carrot cure” really could be the key to avoiding type 2 diabetes.
More research is planned, but you don’t have to wait around for those studies to be done. You can start getting more vitamin A today.
By far the best way to raise your vitamin A levels is through diet. There are two types of vitamin A. Retinol, or preformed vitamin A, is found in meat, poultry, fish and dairy. And beta-carotene, or pro-vitamin A, which you can get in many fruits and veggies.
Foods rich in this vital vitamin include:
- carrots
- beef liver
- sweet potatoes
- kale
- spinach
- broccoli
- sweet red peppers
- tuna fish
- mango
You can’t get too much vitamin-A through your diet so eat as much of these healthy foods as you like.
But as we all know getting too much of a good thing is a bad idea, and that holds true for too much vitamin A as well. So skip the supplements and stick with those delicious and nutritious vitamin-rich foods instead.
Get more vitamin A today to help avoid a diabetes diagnosis tomorrow.
References:
1. “Vitamin A Deficiency Causes Hyperglycemia and Loss of Pancreatic β-Cell Mass,” The Journal of Biological Chemistry, 290, 1456-1473
2. “Anti-diabetic action of all-trans retinoic acid and the orphan G protein coupled receptor GPRC5C in pancreatic β-cells,” Endocrine Journal, 2017; 64 (3): 325
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