OBJECTIVETo investigate the effects of 54G/C polymorphism of sterol regulatory element-binding protein-1c gene (SREBP-1c) on serum lipid ratios and their response to high-carbohydrate/low-fat (HC/LF) diet in healthy youth.

METHODSAfter a regular diet for 7 days of wash-out, 56 healthy youth (22.89 +/- 1.80 yrs) were given HC/LF diet for 6 days. The regular diet contained 54% carbohydrate, 15% protein, and 31% fat of the total energy. The HC/LF diet contained 70% carbohydrate, 15% protein, and 15% fat of the total energy. The serum lipids and glucose were measured on the 1st, 8th and 14th days. The ratios of TG/HDL-C, log (TG/HDL-C), TC/HDL-C, and LDL-C/HDL-C were calculated. The 54G/C polymorphism of SREBP-1c gene was analyzed by PCR-RFLP method.

RESULTSNo significant difference was found in lipid ratios and glucose at baseline and after regular diet in subjects with different genotypes in either the whole studied population or in males or females only. However, after HC/LF diet, LDL-C/HDL-C was significantly lower in females carrying the C allele than those of GG homozygotes (P< 0.05). Compared with those before HC/LF diet, TC/HDL-C and LDL-C/HDL-C were significantly decreased in all the subjects (P< 0.05). When gender was taken into account, significant increase of TG/HDL-C and log(TG/HDL-C) was found only in females with GG genotype (P< 0.05). All the subjects experienced significant decrease of TC/HDL-C and LDL-C/HDL-C regardless of their genders and genotypes (P< 0.05).

CONCLUSIONThe 54G/C polymorphism of SREBP-1c gene can influence the response of TG/HDL-C and log(TG/HDL-C) to HC/LF diet in females. The C allele may be a protective factor to prevent the increase of TG induced by HC/LF diet in females.

Adult ; Dietary Carbohydrates ; pharmacology ; Dietary Fats ; pharmacology ; Female ; Gene Frequency ; Genotype ; Health ; Humans ; Lipids ; blood ; Male ; Polymorphism, Single Nucleotide ; Sex Characteristics ; Sterol Regulatory Element Binding Protein 1 ; genetics ; Young Adult

This study was conducted to evaluate whether the composition of carbohydrate or fat diet affects insulin resistance by measuring the muscle glucose transport rate. Both high-sucrose and high-starch diet with or without high-fat decreased insulin-stimulated glucose transport, but there were no significant differences among groups. Calorie intake in both high-sucrose and high-starch diet groups was higher than in chow group. The high-fat high-sucrose diet induced decrease in insulin-stimulated glucose transport was partially improved by supplement with fish oil. Calorie intake in high-fat high-sucrose and fish oil supplemented groups was higher than in chow group. The decreased insulin-stimulated glucose transport was accompanied by the increase in visceral fat mass, plasma triglyceride and insulin levels. These changes were improved by the supplement with fish oil. These results demonstrate that the composition of fat in diet is clearly instrumental in the induction of muscle insulin resistance. However, in high carbohydrate diet, it is likely that the amount of calorie intake may be a more important factor in causing insulin resistance than the composition of carbohydrate. Thus, the compositions of carbohydrate and fat in diet differentially affect on muscle insulin resistance.
Animals ; Blood Glucose/metabolism ; Body Weight ; Diet ; Dietary Carbohydrates/*pharmacology ; Dietary Fats/*pharmacology ; Dietary Supplements ; Energy Intake/drug effects ; Fish Oils/pharmacology ; Insulin/blood ; Insulin Resistance/*physiology ; Intra-Abdominal Fat/drug effects/metabolism ; Male ; Muscle, Skeletal/*drug effects/physiology ; Rats ; Rats, Sprague-Dawley

Acetyl CoA carboxylase contents in liver cytosol of rats refed a high carbohydrate diet or injected with insulin were measured by an immunoassay method in order to evaluate the effects of dietary carbohydrate and insulin treatment on the control in the amount of acetyl CoA carboxylase. Acetyl CoA carboxylase was purified 1,552 folds with a specific activity of 3.88 units/mg protein from livers of rats refed a high carbohydrate diet for 3 days following a 3-day fasting and the antibody was generated against the purified acetyl CoA carboxylase in a rabbit. Treatment of insulin (1.5 units/100g BW) and a high carbohydrate diet increased the amount of acetyl CoA carboxylase in liver cytosol by 3 times and 10 times, respectively, when compared to the enzyme content found in the control. The synthetic ratio of acetyl CoA carboxylase to total cytosolic proteins was 4 times higher in the insulin-treated group and 10 times higher in the high carbohydrated diet-treated group than the control group. The polysomal RNA contents in liver cytosols were 279% of the control in the insulin-treated group and 365% of the control in the high carbohydrate diet group. Also, the nascent chain of acetyl CoA carboxylase in polysome were 158% of the control in the insulin-treated group and 311% of the control in the high carbohydrate treated group. From these results, it is assumed that the increase of acetyl CoA carboxylase content in the rat liver cells by insulin treatment, or high carbohydrate diet refeeding has resulted from the increased polysomal acetyl CoA carboxylase mRNA, which is directly related to the biosynthesis of this enzyme.
Acetyl-CoA Carboxylase/*metabolism ; Animal ; Cytosol/*metabolism ; Dietary Carbohydrates/*administration and dosage ; Insulin/*pharmacology ; Ligases/*metabolism ; Liver/enzymology/*metabolism ; Male ; RNA, Messenger/*metabolism ; Rats ; Rats, Inbred Strains ; Support, Non-U.S. Gov't

Acetyl CoA carboxylase contents in liver cytosol of rats refed a high carbohydrate diet or injected with insulin were measured by an immunoassay method in order to evaluate the effects of dietary carbohydrate and insulin treatment on the control in the amount of acetyl CoA carboxylase. Acetyl CoA carboxylase was purified 1,552 folds with a specific activity of 3.88 units/mg protein from livers of rats refed a high carbohydrate diet for 3 days following a 3-day fasting and the antibody was generated against the purified acetyl CoA carboxylase in a rabbit. Treatment of insulin (1.5 units/100g BW) and a high carbohydrate diet increased the amount of acetyl CoA carboxylase in liver cytosol by 3 times and 10 times, respectively, when compared to the enzyme content found in the control. The synthetic ratio of acetyl CoA carboxylase to total cytosolic proteins was 4 times higher in the insulin-treated group and 10 times higher in the high carbohydrated diet-treated group than the control group. The polysomal RNA contents in liver cytosols were 279% of the control in the insulin-treated group and 365% of the control in the high carbohydrate diet group. Also, the nascent chain of acetyl CoA carboxylase in polysome were 158% of the control in the insulin-treated group and 311% of the control in the high carbohydrate treated group. From these results, it is assumed that the increase of acetyl CoA carboxylase content in the rat liver cells by insulin treatment, or high carbohydrate diet refeeding has resulted from the increased polysomal acetyl CoA carboxylase mRNA, which is directly related to the biosynthesis of this enzyme.
Acetyl-CoA Carboxylase/*metabolism ; Animal ; Cytosol/*metabolism ; Dietary Carbohydrates/*administration and dosage ; Insulin/*pharmacology ; Ligases/*metabolism ; Liver/enzymology/*metabolism ; Male ; RNA, Messenger/*metabolism ; Rats ; Rats, Inbred Strains ; Support, Non-U.S. Gov't

OBJECTIVETo study the effect of ginsenoside Rb1 on GSKbeta/IDE signal transduction pathway and Abeta protein secretion in hippocampal neurons of high glucose-treated rats.

METHODHippocampal neurons of 24 h-old newly born SD rats were primarily cultured, inoculated in culture medium under different conditions, and then divided into the normal group, the high glucose group, the LiCl group and the Rb1 group. After being cultured for 72 h, the expressions of their phosphorylated GSK3beta, total GSK3beta and IDE protein were detected by Western blotting analysis. The mRNA expressions of GSK3beta and IDE were determined by RT-PCR. The ELISA assay was used to detect the secretion of Abeta protein in cell supernatant.

RESULTCompared with the normal group, the high glucose group showed increase in the p/tGSK3beta protein ratio and the secretion of Abeta protein and decrease in IDE protein and mRNA (P < 0.05). Compared with the high glucose group, both Rb1 and LiCl groups showed decrease in the p/tGSK3beta protein ratio and the expression of Abeta protein and increase in IDE protein and mRNA expression (P < 0.05). Compared with the LiCl group, the Rb1 group showed no significant difference in the expressions of p/tGSK3beta protein, IDE protein, mRNA and Abeta protein expression. In addition, the GSK3beta mRNA expression of the four groups had no significant difference.

CONCLUSIONGinsenoside Rb1 may reduce the secretion of Abeta protein in hippocampal neurons by reducing the phosphorylation of GSK3beta, down-regulating the ratio of pGSK3beta/GSK3beta and upregulating the expression of IDE.

Amyloid beta-Peptides ; genetics ; metabolism ; secretion ; Animals ; Dietary Carbohydrates ; adverse effects ; Gene Expression Regulation ; drug effects ; Ginsenosides ; pharmacology ; Glucose ; adverse effects ; Glycogen Synthase Kinase 3 ; genetics ; metabolism ; Glycogen Synthase Kinase 3 beta ; Hippocampus ; cytology ; Insulin ; metabolism ; Insulysin ; genetics ; metabolism ; Neurons ; cytology ; drug effects ; metabolism ; secretion ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; drug effects