Such_Saturation
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Atg7 complementation resulted in reduced hepatic fatty acid infiltration ( Figures 6A and 6B), liver triglyceride content ( Figure 6C), and serum insulin level ( Figure 6D). There was a modest increase in serum triglyceride, but not free fatty acid levels, in mice expressing exogenous Atg7 ( Figures S5C and S5D). It is possible that enhanced autophagy reduced lipid accumulation through an increase in lipid metabolism, as proposed by Singh et al. (2009). [http://www.sciencedirect.com/science/article/pii/S1550413110001166]
Sinha et al. report on a study demonstrating that caffeine may be just such an ideal intervention to protect against FLD by enhancing lipophagy and mitochondrial-β oxidation simultaneously.[14] By using a series of autophagic flux assays, they demonstrated that caffeine induces autophagic flux in human hepatoma cells, primary cultured hepatocytes, and mouse livers. They further found that caffeine-induced autophagosomes often contain LDs, suggesting the induction of lipophagy. Metabolomic analysis of hepatic acylcarnitines revealed an increase of hepatic lipolysis by caffeine treatment. More important, caffeine increased mitochondrial β-oxidation activity and inhibited hepatic steatosis in a high-fat-diet-fed mouse model. Interestingly, they found that small interfering RNA knockdown of Atg5, an essential autophagy gene required for biogenesis of autophagosomes, inhibited caffeine-induced mitochondrial β-oxidation and mitochondrial bioenergetics. Selective removal of damaged mitochondria by mitophagy may help to maintain better quality of mitochondria and thus enhance mitochondrial β-oxidation and mitochondrial bioenergetics. [http://onlinelibrary.wiley.com/doi/10.1002/hep.26736/full] (see Lithium makes the weaker mithochondria die off)
circadian regulation of C/EBPβ and autophagy is disrupted in mice lacking a functional liver clock. [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3243590/]
Lithium, a drug used to treat bipolar disorders, has a variety of neuroprotective mechanisms, including autophagy regulation [http://www.ncbi.nlm.nih.gov/pubmed/24738557]
The data suggest that exogenous lithium stimulates triglyceride metabolism since liver triglycerides decreased concomitant with an increase in serum free fatty acid. [http://jn.nutrition.org/content/104/10/1242.full.pdf]
Sinha et al. report on a study demonstrating that caffeine may be just such an ideal intervention to protect against FLD by enhancing lipophagy and mitochondrial-β oxidation simultaneously.[14] By using a series of autophagic flux assays, they demonstrated that caffeine induces autophagic flux in human hepatoma cells, primary cultured hepatocytes, and mouse livers. They further found that caffeine-induced autophagosomes often contain LDs, suggesting the induction of lipophagy. Metabolomic analysis of hepatic acylcarnitines revealed an increase of hepatic lipolysis by caffeine treatment. More important, caffeine increased mitochondrial β-oxidation activity and inhibited hepatic steatosis in a high-fat-diet-fed mouse model. Interestingly, they found that small interfering RNA knockdown of Atg5, an essential autophagy gene required for biogenesis of autophagosomes, inhibited caffeine-induced mitochondrial β-oxidation and mitochondrial bioenergetics. Selective removal of damaged mitochondria by mitophagy may help to maintain better quality of mitochondria and thus enhance mitochondrial β-oxidation and mitochondrial bioenergetics. [http://onlinelibrary.wiley.com/doi/10.1002/hep.26736/full] (see Lithium makes the weaker mithochondria die off)
circadian regulation of C/EBPβ and autophagy is disrupted in mice lacking a functional liver clock. [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3243590/]
Lithium, a drug used to treat bipolar disorders, has a variety of neuroprotective mechanisms, including autophagy regulation [http://www.ncbi.nlm.nih.gov/pubmed/24738557]
The data suggest that exogenous lithium stimulates triglyceride metabolism since liver triglycerides decreased concomitant with an increase in serum free fatty acid. [http://jn.nutrition.org/content/104/10/1242.full.pdf]