Naturally occurring bile acid can blunt statin-induced diabetes

Subject: Science and tech

Section: Health

Context:

A study from China has discovered that ursodeoxycholic acid (UDCA) can counteract the side effect of statins, which is the tendency to induce glucose intolerance and diabetes.

Statins:

Statins are a class of medications that reduce illness and mortality in people who are at high risk of cardiovascular disease. They are the most commonly prescribed cholesterol-lowering drugs and are also known as HMG-CoA reductase inhibitors.
Statins, widely prescribed to reduce cardiovascular disease risk by lowering LDL (low-density lipoprotein) cholesterol, have been linked to an increased diabetes risk despite their global prevalence as essential and top-selling medications.
Statins are on the World Health Organization’s list of essential medicines and among the most sold drugs worldwide.

Mechism behind induced glucose intolerance:

Statins can induce glucose intolerance and even lead to diabetes in some individuals. Despite these side effects, the benefits of statins are deemed to outweigh the risks, which has kept them in widespread use.
A study identified a mechanism behind this effect, involving the bile acid UDCA.
Researchers observed that individuals taking atorvastatin showed a decrease in Clostridium bacteria in their faeces and had altered bile acid profiles in their serum and faeces, suggesting a potential link to the development of glucose intolerance.

Gut microbiome:

Researchers have uncovered that a Clostridium-deficient gut microbiome, influenced by statins, may impair glucose metabolism by inhibiting hydroxysteroid dehydrogenases enzymes and reducing UDCA levels.
This was further explored through a study on mice over 12 weeks, suggesting that alterations in the gut microbiome could affect bile acid synthesis and glucose regulation.
A human trial with statin users given UDCA showed improved HbA1C levels, indicating better glucose homeostasis without affecting statins’ lipid-lowering benefits.

Source: TH