171 research outputs found
Kheper, a Novel ZFH/δEF1 Family Member, Regulates the Development of the Neuroectoderm of Zebrafish (Danio rerio)
AbstractKheper is a novel member of the ZFH (zinc-finger and homeodomain protein)/δEF1 family in zebrafish. kheper transcripts are first detected in the epiblast of the dorsal blastoderm margin at the early gastrula stage and kheper is expressed in nearly all the neuroectoderm at later stages. kheper expression was expanded in noggin RNA-injected embryos and also in swirl mutant embryos and was reduced in bmp4 RNA-injected embryos and chordino mutant embryos, suggesting that kheper acts downstream of the neural inducers Noggin and Chordino. Overexpression of Kheper elicited ectopic expansion of the neuroectoderm-specific genes fkd3, hoxa-1, and eng3, and the ectopic expression of hoxa-1 was not inhibited by BMP4 overexpression. Kheper interacted with the transcriptional corepressors CtBP1 and CtBP2. Overexpression of a Kheper mutant lacking the homeodomain or of a VP16–Kheper fusion protein disturbed the development of the neuroectoderm and head structures. These data underscore the role of Kheper in the development of the neuroectoderm and indicate that Kheper acts as a transcriptional repressor
Improvement of Glucose Metabolism in Patients with Impaired Glucose Tolerance or Diabetes by Long-Term Administration of a Palatinose-Based Liquid Formula as a Part of Breakfast
A palatinose-based liquid formula (palatinose-formula), suppresses postprandial plasma glucose and insulin levels in healthy men. The objective of this study was to investigate the effects of long-term palatinose-formula ingestion on glucose metabolism in patients with impaired glucose tolerance (IGT) or type 2 diabetes. Two patients with IGT and 7 patients with type 2 diabetes participated in the palatinose-formula and dextrin-based liquid formula (dextrin-formula) loading test and long-term palatinose-formula administration study. After a 3-month control period, palatinose-formula (1046 kJ) was ingested daily by patients as a part of breakfast for 5 months. In the loading test, palatinose-formula suppressed postprandial plasma glucose and insulin levels and areas under the curve compared with those after dextrin-formula ingestion. In the long-term study, glycated hemoglobin levels (after 3 months and 5 months of treatment) and serum 8-hydroxydeoxyguanosine levels (after 5 months of treatment) were markedly decreased comparing with those at baseline. Intake of 1046 kJ palatinose-formula as a part of breakfast over a long-term period may be effective for improvement of glucose metabolism in patients with IGT or type 2 diabetes
The Anti-Obesity Effect of the Palatinose-Based Formula Inslow is Likely due to an Increase in the Hepatic PPAR-α and Adipocyte PPAR-γ Gene Expressions
Abdominal obesity is a principal risk factor in the development of metabolic syndrome. Previously, we showed that a palatinose-based liquid formula, Inslow/MHN-01, suppressed postprandial plasma glucose level and reduced visceral fat accumulation better than the standard formula (SF). To elucidate the mechanism of Inslow-mediated anti-obesity effect, expression levels of genes involved in the glucose and lipid metabolism were compared in Inslow- and SF-fed rats. Both fasting plasma insulin level and average islet sizes were reduced in the Inslow group. We also found less abdominal fat accumulation and reduced hepatic triacylglycerol content in the Inslow group. Expression of the β-oxidation enzymes and uncoupling potein-2 (UCP-2) mRNAs in the liver of the Inslow group were higher than the SF group, which was due to a concomitant higher expression of the peroxisome proliferator-activated receptor (PPAR)-α mRNA in the former. Furthermore, expression of the UCP-2 and adiponectin mRNAs in the epididymal fat were higher in the Inslow group than the SF group, and were stimulated by a concomitant increase of the PPAR-γ gene expression in the former. These results strongly suggested that the anti-obesity effect of Inslow was due to an increase in the hepatic PPAR-α and adipocyte PPAR-γ gene expressions
Insulin resistance as early sign of hepatic dysfunction in liver cirrhosis
Glucose intolerance characterized by postprandial hyperglycemia and hyperinsulinemia
is commonly seen in patients with liver cirrhosis (LC). The aim of this study
is to clarify the relation between glucose intolerance and disorder of liver function in
patients with LC. The 75 g oral glucose tolerance test (75 g OGTT) and the hyperinsulinemic
euglycemic clamp combined with 0.2 g/kg oral glucose load (HECGL) were conducted
in 61 patients with LC. Based on the results of 75 g OGTT, the 61 patientswith LCwere divided
into groups, 21 (34.4%) patients with normal glucose tolerance (LC-NGT), 12 (19.7%)
patients with impaired glucose tolerance (LC-IGT) and 28 (45.9%) patients with diabetes
mellitus (LC-DM). Fasting plasma glucose (FPG) level was normal in 50 (82.0%) patients
with LC. All patients with LC showed insulin resistance in both peripheral (skeletal and
adipose) and hepatic tissues evaluated by HECGL, although significant correlation between
the degree of glucose intolerance and the severity of hepatic dysfunction was not observed.
Insulin resistance in both liver and peripheral tissues is the early sign in the patients with
LC. This fact indicates that nutritional care from early stages of LC would be necessary in
the patients
Resistivity anisotropy measured using four probes in epitaxial graphene on silicon carbide
The electronic transport of epitaxial graphene on silicon carbide is anisotropic because of the anisotropy of the surface structure of the substrate. In this Letter, we present a new method for measuring anisotropic transport based on the van der Pauw method. This method can measure anisotropic transport on the macroscopic scale without special equipment or device fabrication. We observe an anisotropic resistivity with a ratio of maximum to minimum of 1.62. The calculated maximum mobility is 2876cm2·V-1·s-1, which is 1.43 times higher than that obtained by the standard van der Pauw method
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