Biotin is mainly required as a coenzyme for carboxylation reactions and the main examples are carboxylation of-i) pyruvate to oxaloacetate (first step of gluconeogenesis); ii) Acetyl co A to Malonyl co A (first step of fatty acid synthesis) and iii) Propionyl co A to D-Methyl malonyl co A (in the conversion of propionyl co A to Succinyl co A to gain entry to TCA cycle). In biotin deficiency, out of the given options, defective fatty acid synthesis is the most suited option because of the impaired conversion of acetyl co A to malonyl co A.
The groundbreaking study from Backhed and colleagues in 2004 not only found that mice raised germ free and subsequently colonized with gut flora from normal mice quickly developed increased fat stores, but also that they developed insulin In comparison with germ-free mice, the formerly germ-free mice that were colonized with gut flora had increased fasting serum glucose concentration as well as increased leptin and insulin concentrations. The possible influence of gut bacteria on the development of insulin resistance may be exerted through inflammatory The short-chain fatty acids and other molecules that gut bacteria produce as a metabolic by-product can act as inflammatory triggers by binding to toll-like receptors, which begin a cascade of inflammatory signaling. Human studies support a connection between gut bacteria and diabetes: People with type 2 diabetes have been found to have reduced levels of Firmicutes in their gut bacteria profiles compared with those without Currently, it’s unclear whether a gut flora profile is directly related to insulin resistance or indirectly related and dependent on the development of obesity.