In people with fatty liver disease, a person’s fat goes to his liver instead of going to his adipose tissue, either because of a lack of fat stores, which occurs in lipodystrophy (a rare genetic disease), or because fat stores are full, something seen in obese people.
One-third of these people will continue to develop non-alcoholic steatopathy (NASH), an advanced form of fatty liver disease caused by progressive inflammation and scarring of the liver.
In 2002, University of Michigan endocrinologist Elif Oral published the discovery that patients with severe lipodystrophy lacked leptin, a hormone that helps control appetite and control weight gain. When leptin was given as a supplement, severe metabolic abnormalities in patients with NASH improved significantly.
Oral further studied the role of leptin in more common forms of NASH. Nearly two decades later, her research team found that either due to leptin deficiency or partial lipodystrophy, patients with NASH and relatively low leptin levels could mobilize fat outside their liver, and reverse their condition by receiving treatment with leptin.
As described in Med: Cell Press, Oral and her team conducted two trials studying nine male patients with NASH and low leptin levels (less than 9 ng / ml) and 23 patients with partial lipodystrophy and NASH. Both groups were treated with leptin for one year.
“Not all NASHs are the same. “There is a huge distribution of leptin levels in this patient population,” Oral said. “High levels of leptin, which are observed in obesity, may in fact be causative of NASH, so it was important to carefully select participants for the test for low levels.”
After liver biopsy, both groups were found to have reduced liver fat and lower NASH scores after 12 months of leptin treatment. Patients also had improved insulin sensitivity and body weight.
Source: Zougla.gr by www.zougla.gr.
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