The Supply of Glucose to the Body during Fasting Is Made Possible by the Effect of Vitamin B2 on the Peroxisome Proliferator-Activated Receptor Αlpha

During fasting, a lot of energy is expended but not replaced as the body’s coping mechanisms get activated. Glucose, which is mostly derived from carbs, is the main source of energy. When the body requires it, the liver and muscles release the glucose they have stored into circulation. Fasting generally works by inducing adaptive cellular stress responses, which improve the body’s capacity to handle more intense stress and fend off disease processes. A lot of mechanisms are involved in this process including the action of vitamin B2 on PPARα. The cofactor versions of the vitamin which are Flavin mononucleotide(FMN) and Flavin adenine dinucleotide(FAD) interact with PPARα to regulate glucose metabolism and ultimately provide energy.

Vitamin B2

Vitamin B2

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 A significant difference is made by vitamin B2

A deficiency of vitamin B2 can lead to an imbalance in metabolism leading to various inborn errors of metabolism that induce hepatic steatosis, lipodystrophy, and intolerance to fasting.

A study was carried out on lab rats to determine the importance of the vitamin in the metabolism of glucose and its effect on PPARα. Here, we define outcomes of vitamin B2 depletion resembling inborn errors of metabolism of flavoprotein deficiency and transcriptional pathways that preserve glucose availability in fasting mice. All mice were kept in a facility that was barrier-specific, pathogen-free, and allowed unrestricted access to vitamin b2 deficient food(B2D) and water. After 4 weeks of administering B2D, hypoglycemia and accumulation of fat in the liver ensued. On result analysis, 99% vitb2 depletion was discovered which was enough to reduce levels by 70%. A considerable amount of weight loss was noticed and it was also discovered that B2D reduced PPARα-regulated flavoprotein genes. These features suggest that hepatic glucose metabolism is directly impacted by FAD deficiency and The availability of fasting glucose is maintained by hepatic FAD pools via PPAR activation.

Furthermore, fenofibrate was administered to the test rats. This is a fibrate drug that acts specifically on PPARα to lower blood lipids and treat hypertriglyceridemia. It was observed that under B2D circumstances, fenofibrate elevated blood sugar levels and decreased hepatic steatosis.

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Clinical significance 

The role of vitamin B2 is clinically significant. The availability of the vitamin maintains a balance in the metabolism of glucose and fatty acids. A deficiency can lead to various inborn errors. The advent of vitamin B2 supplements and even drugs like fenofibrate that can stimulate PPARα improves the situation and increases life expectancy.


The human body continually needs an ample supply of energy to keep up with life. Mechanisms have been put in place to achieve this. In conclusion, knowing how hypoglycemia and fatty liver are overcome by nuclear receptor modulation of flavoprotein activity and FAD pool distribution is important for implementing metabolic therapies and future therapeutic techniques.

Read Also: Fasting Increases Production of Anti-Aging Molecule


Vitamin B2 enables peroxisome proliferator-activated receptor α regulation of fasting glucose availability | bioRxiv



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