No abstract

No abstract

No abstract

No abstract

The flavonoid luteolin has various pharmacological activities. However, few studies exist on the in vivo mechanism underlying the actions of luteolin in hepatic steatosis and obesity. The aim of the current study was to elucidate the action of luteolin on obesity and its comorbidity by analyzing its transcriptional and metabolic responses, in particular the luteolin-mediated cross-talk between liver and adipose tissue in diet-induced obese mice. C57BL/6J mice were fed a normal, high-fat, and high-fat + 0.005% (weight for weight) luteolin diet for 16 weeks. In high fatfed mice, luteolin improved hepatic steatosis by suppressing hepatic lipogenesis and lipid absorption. In adipose tissue, luteolin increased PPARg protein expression to attenuate hepatic lipotoxicity, which may be linked to the improvement in circulating fatty acid (FA) levels by enhancing FA uptake genes and lipogenic genes and proteins in adipose tissue. Interestingly, luteolin also upregulated the expression of genes controlling lipolysis and the tricarboxylic acid (TCA) cycle prior to lipid droplet formation, thereby reducing adiposity. Moreover, luteolin improved hepatic insulin sensitivity by suppressing SREBP1 expression that modulates Irs2 expression through its negative feedback and gluconeogenesis. Luteolin ameliorates the deleterious effects of diet-induced obesity and its comorbidity via the interplay between liver and adipose tissue.Obesity is characterized by excessive fat accumulation and is associated with metabolic complications such as adiposity, dyslipidemia, insulin resistance, and steatohepatitis. The liver is one of the major organs responsible for metabolizing fats from the diet. Dysregulation of lipid metabolism in the liver induces abnormal accumulation of lipids and the subsequent formation of lipid droplets (LDs), known as hepatic steatosis. Hepatic steatosis is common in obese individuals and is strongly linked to insulin resistance (1,2). Adipose tissue is also a critical component of metabolic control and is an endocrine organ that secretes a number of adipokines known to mediate lipid metabolism, inflammation, and insulin sensitivity (3). Although the complex relationship between adiposity and hepatic steatosis has not been completely elucidated, dysregulation of lipid metabolism in the liver and adipose tissue may be involved in the pathogenesis of adiposity as well as its associated metabolic complications. One hypothesis for the explanation of a link between visceral adiposity and hepatic steatosis and insulin resistance is the "portal hypothesis," which proposes that a high rate of lipolysis of the visceral adipose tissue can lead to an increased delivery of free fatty acids (FFAs) to the liver via the portal vein, and that chronic exposure of the liver to elevated FFAs can promote hepatic steatosis and hepatic insulin resistance (4,5). However, it is still unclear how visceral adiposity is associated with hepatic steatosis and insulin resistance, in particular at the level of transcriptional changes that occur in ...

No abstract

No abstract

Aims: The objective of the present study was to determine the optimal culture conditions for exo-biopolymer production by Cordyceps militaris in shake¯ask culture. Methods and Results: The optimal temperature and initial pH for both mycelial growth and exo-biopolymer production by Cordyceps militaris in shake¯ask culture were found to be 20°C and 6á0, respectively. Sucrose (40 g l ±1 ) and corn steep powder (10 g l ±1 ) were the most suitable carbon and nitrogen source for both mycelial growth and exo-biopolymer production. Conclusions: Under optimal culture conditions, the maximum exo-biopolymer concentration in a 5-l jar fermenter indicated 10á3 g l ±1 , which was approximately three times higher than that in shake¯ask culture. Signi®cance and Impact of the Study: This process can have a signi®cant impact on the industrial scale when sucrose and corn steep powder were used as carbon and nitrogen source.