Corticosteroids have been used as drug treatment for some time. Lewis Sarett of Merck & Co. was the first to synthesize cortisone, using a complicated 36-step process that started with deoxycholic acid, which was extracted from ox bile .  The low efficiency of converting deoxycholic acid into cortisone led to a cost of US $200 per gram. Russell Marker , at Syntex , discovered a much cheaper and more convenient starting material, diosgenin from wild Mexican yams . His conversion of diosgenin into progesterone by a four-step process now known as Marker degradation was an important step in mass production of all steroidal hormones, including cortisone and chemicals used in hormonal contraception .  In 1952, . Peterson and . Murray of Upjohn developed a process that used Rhizopus mold to oxidize progesterone into a compound that was readily converted to cortisone.  The ability to cheaply synthesize large quantities of cortisone from the diosgenin in yams resulted in a rapid drop in price to US $6 per gram, falling to $ per gram by 1980. Percy Julian's research also aided progress in the field.  The exact nature of cortisone's anti-inflammatory action remained a mystery for years after, however, until the leukocyte adhesion cascade and the role of phospholipase A2 in the production of prostaglandins and leukotrienes was fully understood in the early 1980s.
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.
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