Hexoses accumulate to high concentrations （-200 mM） in storage parenchyma cells of tomato fruit. Hexoses are sourced from the fruit apoplasm as hydrolysis products of phloem-imported sucrose. Three hexose transporte...Hexoses accumulate to high concentrations （-200 mM） in storage parenchyma cells of tomato fruit. Hexoses are sourced from the fruit apoplasm as hydrolysis products of phloem-imported sucrose. Three hexose transporters （LeHT1, LeHT2, LeHT3）, expressed in fruit storage parenchyma ceils, may contribute to hexose uptake by these cells. An analysis of their full-length sequences demonstrated that all three transporters belong to the STP subfamily of monosaccharide transporters that localize to plasma membranes. Heterologous expression of LeHT1 （and previously LeHT2, Gear et al., 2000）, but not LeHT3, rescued a hexose transportimpaired yeast mutant when raised on glucose or fructose as the sole carbon source. Biochemically, LeHT1, similarly to LeHT2, exhibited transport properties consistent with a high- affinity glucose/H^＋ symporter. Significantly, LeHT1 and LeHT2 also functioned as low-affinity fructose/H^＋ symporters with apparent Km values commensurate with those of fruit tissues. A substantial reduction （80-90%） in fruit expression levels of all LeHT genes by RNAi-mediated knockdown caused a 55% decrease in fruit hexose accumulation. In contrast, photoassimilate production by source leaves and phloem transport capacity to fruit were unaffected by transporter knockdown. Collectively, these findings demonstrate that LeHTs play key roles in driving accumulation of hexoses into storage parenchyma cells during tomato fruit development.展开更多
The metabolic syndrome, one of the most common clinical conditions in recent times, represents a combination of cardiometabolic risk determinants, including central obesity, glucose intolerance, insulin resistance, d... The metabolic syndrome, one of the most common clinical conditions in recent times, represents a combination of cardiometabolic risk determinants, including central obesity, glucose intolerance, insulin resistance, dyslipidemia, non-alcoholic fatty liver disease and hypertension. Prevalence of the metabolic syndrome is rapidly increasing worldwide as a consequence of common overnutrition and consequent obesity. Although a unifying picture of the pathomechanism is still missing, the key role of the pre-receptor glucocorticoid activation has emerged recently. Local glucocorticoid activation is catalyzed by a triad composed of glucose-6-phosphate-transporter, hexose-6-phosphate dehydrogenase and 11β-hydroxysteroid dehydrogenase type 1 in the endoplasmic reticulum. The elements of this system can be found in various cell types, including adipocytes and hepatocytes. While the contribution of glucocorticoid activation in adipose tissue to the pathomechanism of the metabolic syndrome has been well established, the relative importance of the hepatic process is less understood. This review summarizes the available data on the role of the hepatic triad and its role in the metabolic syndrome, by confronting experimental findings with clinical observations.展开更多
文摘Hexoses accumulate to high concentrations （-200 mM） in storage parenchyma cells of tomato fruit. Hexoses are sourced from the fruit apoplasm as hydrolysis products of phloem-imported sucrose. Three hexose transporters （LeHT1, LeHT2, LeHT3）, expressed in fruit storage parenchyma ceils, may contribute to hexose uptake by these cells. An analysis of their full-length sequences demonstrated that all three transporters belong to the STP subfamily of monosaccharide transporters that localize to plasma membranes. Heterologous expression of LeHT1 （and previously LeHT2, Gear et al., 2000）, but not LeHT3, rescued a hexose transportimpaired yeast mutant when raised on glucose or fructose as the sole carbon source. Biochemically, LeHT1, similarly to LeHT2, exhibited transport properties consistent with a high- affinity glucose/H^＋ symporter. Significantly, LeHT1 and LeHT2 also functioned as low-affinity fructose/H^＋ symporters with apparent Km values commensurate with those of fruit tissues. A substantial reduction （80-90%） in fruit expression levels of all LeHT genes by RNAi-mediated knockdown caused a 55% decrease in fruit hexose accumulation. In contrast, photoassimilate production by source leaves and phloem transport capacity to fruit were unaffected by transporter knockdown. Collectively, these findings demonstrate that LeHTs play key roles in driving accumulation of hexoses into storage parenchyma cells during tomato fruit development.
基金Supported by the János Bolyai Research Scholarship of the Hungarian Academy of Sciences to Csala M
文摘 The metabolic syndrome, one of the most common clinical conditions in recent times, represents a combination of cardiometabolic risk determinants, including central obesity, glucose intolerance, insulin resistance, dyslipidemia, non-alcoholic fatty liver disease and hypertension. Prevalence of the metabolic syndrome is rapidly increasing worldwide as a consequence of common overnutrition and consequent obesity. Although a unifying picture of the pathomechanism is still missing, the key role of the pre-receptor glucocorticoid activation has emerged recently. Local glucocorticoid activation is catalyzed by a triad composed of glucose-6-phosphate-transporter, hexose-6-phosphate dehydrogenase and 11β-hydroxysteroid dehydrogenase type 1 in the endoplasmic reticulum. The elements of this system can be found in various cell types, including adipocytes and hepatocytes. While the contribution of glucocorticoid activation in adipose tissue to the pathomechanism of the metabolic syndrome has been well established, the relative importance of the hepatic process is less understood. This review summarizes the available data on the role of the hepatic triad and its role in the metabolic syndrome, by confronting experimental findings with clinical observations.
