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Increased levels of triglycerides (IHTG) in the liver are a signature feature of non-alcoholic fatty liver disease (NAFLD), which decreases after weight loss.
new fat production (DNL) in the liver promotes fat degeneration in NAFLD patients.
, the physiological factors that stimulate liver DNL and the effects of weight loss on liver DNL are not yet known, a study published in J Clin Invest explores.
study included participants in thinness (n s 14), normal IHTG levels of obesity (n s 26) and non-alcoholic fatty liver (n s 27) to determine liver DNL, 24-hour combined plasma insulin and glucose concentrations, and liver and systemic insulin sensitivity.
to correct the adipose tissue DNL, the liver DNL was evaluated using radonized water.
the liver and systemic insulin sensitivity were assessed using the hyperinsepemia-glycemic pliers procedure with glucose tracer infusion.
the obese-NAFLD group were also assessed before and after a diet-induced 10 percent weight loss.
results showed that liver DNL contributed 11%, 19% and 38% to IHTG-palmic acid, respectively, in the thin, obese and obesity-NAFLD groups.
liver DNL was inversely related to liver and systemic insulin sensitivity, but directly related to 24-hour plasma glucose and insulin concentrations.
weight loss reduced IHTG levels, while liver DNL and 24-hour plasma glucose and insulin concentrations decreased.
, these data show that liver DNL is an important regulator of IHTG content, and that increased circulating glucose and insulin stimulate liver DNL in patients with non-alcoholic fatty liver disease.
weight loss can reduce IHTG levels in part by reducing liver DNL.
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