Animals ; Dietary Carbohydrates ; administration & dosage ; Dietary Fats ; administration & dosage ; Dietary Proteins ; administration & dosage ; Humans ; Malnutrition ; complications ; Obesity ; etiology ; Trace Elements ; administration & dosage

This study was designed to investigate the relationship between nutritional intake and caries experience of junior high school students. The sample consisted of 295 boys and 356 girls in Kangwha county. Dependent variables were total caries experience, occlusal surface caries experience, smooth surface caries experience and DMFS score (Decayed, Missing, Filling Tooth Surface score). Independent variables such as pit and fissure retentiveness of first molars, oral hygiene status, intraoral acidogenicity were also measured by dentists. Other independent variables such as toothbrushing habits, socioeconomic conditions, between-meal eating habits, and daily nutritional intake were determined during an interview. Univariate and multivariate analysis was performed to evaluate how nutritional intake influences caries experience. The results were as follows: 1. The most influential factor on dental caries experience was pit and fissure retentiveness. 2. Dietary fiber and potassium were the significant nutritional factors on total caries experience and occlusal caries experience, and niacin was the significant nutritional factor on smooth surface caries. 3. DMFS score was positively associated with the daily amount of carbohydrate and niacin intake, and negatively associated with total energy intake. The above results suggested that pit and fissure retentiveness was the most influential factor on caries experience. However, in this study, the intake of potassium and niacin was identified to influence the caries experience in addition to confirming the well-known relationship between fiber and carbohydrate intake.
Adolescence ; Child ; Dental Caries/etiology* ; Diet* ; Dietary Carbohydrates/administration & dosage ; Dietary Fiber/administration & dosage ; Energy Intake ; Female ; Human ; Male ; Oral Hygiene

Animals ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; genetics ; metabolism ; Diet, High-Fat ; Dietary Carbohydrates ; administration & dosage ; Dietary Fats ; administration & dosage ; Lipoproteins, IDL ; blood ; Liver ; metabolism ; Male ; RNA, Messenger ; genetics ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Triglycerides ; blood

OBJECTIVETo investigate the influence of short-term high-fat diet (HFD) on glucose and lipid metabolism in male Han Chinese with type 2 diabetes mellitus (T2DM).

METHODSMiddle-aged T2DM men supported with solely diet or diet and metformin were enrolled into the study. The design was an unblinded crossover design. Each of the subjects randomly received one from two types of isocalorie (8786.4 kJ/d) standard diet for three consecutive days on two occasions, with a 6-week wash-out period in between. The component ratios of fat, carbohydrate, and protein were 50%, 35%, and 15% vs. 25%, 60%, and 15% in patients administered with HFD or high carbohydrate diet (HCD). The 24-hour blood samples during the third day were collected. On the morning of the forth day an intravenous glucose tolerance test (IVGTT) was conducted with 25g of glucose.

RESULTSAccording to the determination results of 24-hour profile samples, HFD resulted in a markedly increased circulating level of non-esterified fatty acid (NEFA) as compared to HCD (P < 0.001). Nearly significant higher (P = 0.056) FPG was observed 72 hours after the administration of HFD. Circulating insulin levels were comparable between the two diets. A significantly higher HDL-C was also observed after HFD administration (P < 0.05). As assessed by the IVGTT, acute insulin response of glucose (AIRg) tended to increase after the HFD administration (P = 0.06). Fasting plasma glucagons (GLG) level and AUC(Glucagon) during breakfast period (8:00-12:00) were significantly higher after HFD administration than that of after HCD administration.

CONCLUSIONSShort-term HFD induced the increase of NEFA with lower glucose exposure to the patietns. Fasting plasma glucose increased at the fourth day without remarkable changes of insulin levels which may be due to the increase of hepatic glucose output after HFD administration. The short-term HFD in our study induced early stage of insulin resistance. GLG seemed to play a role in this procedure. beta-cell dysfunction may need a longer high NEFA exposure.

Adult ; Blood Glucose ; metabolism ; China ; Diabetes Mellitus, Type 2 ; ethnology ; metabolism ; Dietary Carbohydrates ; administration & dosage ; Dietary Fats ; administration & dosage ; Fatty Acids, Nonesterified ; metabolism ; Humans ; Insulin ; metabolism ; Male ; Middle Aged

3-Hydroxybutyric Acid ; blood ; Animals ; Dietary Carbohydrates ; administration & dosage ; Dietary Fats ; administration & dosage ; Dietary Proteins ; administration & dosage ; Disease Models, Animal ; Epilepsy ; diet therapy ; metabolism ; pathology ; Hippocampus ; metabolism ; Kainic Acid ; Ketone Bodies ; metabolism ; Male ; Mossy Fibers, Hippocampal ; pathology ; RNA, Messenger ; analysis ; Rats ; Rats, Sprague-Dawley ; Receptors, Kainic Acid ; analysis ; genetics

This study was designed to investigate the effect of cholestyramine on the formation of pigment gallstones in high carbohydrate diet-fed hamsters and whether that effect occurred because of cholecystokinin action. Forty seven hamsters were divided into three groups: group I(n = 16) was fed on normal rodent chow(43% carbohydrate), group II(n = 14) was fed on a high CHO diet(65% carbohydrate), group III(n = 17) was fed on a high CHO diet containing 4% cholestyramine. Gallstones developed in 0% of group I, 42.9% of group II and 5.9% of group III(P< 0.05, group II vs III). To evaluate the chronic status of cholecystokinin level, the wet weight of pancreas and the average area of pancreatic acinar in microscopic high power field were measured. There was no significant difference between group II and group III in pancreatic weight and average area of pancreatic acinar(P> 0.05). In gallbladder bile analysis, there was also no significant difference between group II and group III in cholesterol, phospholipid, total calcium, total bilirubin and bile acid levels. In conclusion, cholestyramine decreases the frequency of pigment gallstone formation in high CHO diet-fed hamsters, but it is not clear whether the mechanism of cholestyramine decreasing the gallstone formation is due to the action of cholecystokinin.
Animal ; Bilirubin/metabolism ; Cholecystokinin/*analysis ; Cholelithiasis/*pathology ; Cholesterol/metabolism ; Cholestyramine/*administration & dosage ; Dietary Carbohydrates/*administration & dosage ; Female ; Gallbladder/*metabolism/pathology ; Hamsters ; Male ; Mesocricetus ; Organ Weight ; Pancreas/physiopathology ; Phospholipids/metabolism ; Pigmentation ; Support, Non-U.S. Gov't

The regulation of fatty acid synthase in rat liver was investigated at transcriptional and post-transcriptional levels. When rats were fasted for 3 days and refed on a high-carbohydrate diet, the amounts of FAS in liver cytosol began to increase at 12 hours and further increased until 48 hours. The amount of mRNA for FAS began to increase at 6 hours and reached to a maximum level at 12 hours, indicating that the expression of mRNA for FAS precedes the increase of FAS protein pool. After 12 hours the amounts of mRNA gradually decreased and remained at a much lowered level between 24 and 48 hours. The elevated amount of FAS mRNA reflected on the amount of FAS protein in the first 24 hours, but these two parameters were not paralleled thereafter, probably due to the changes in the translational efficiencies. The run-on transcriptional activity of FAS gene began to increase at 4 hours after refeeding a high-carbohydrate diet and further increased to reach a maximum level 25 fold of the initial level at 12 hours, followed by a 16 fold level between 24 and 48 hours. The elevation of run-on transcriptional activity of FAS gene preceded the increase of FAS mRNA in the liver cytosol by 2 hours, and a similar increasing pattern was observed until 12 hours. However, FAS mRNA concentration decreased gradually after 12 hours, while the transcriptional activity remained at a high level until 48 hours. The changes in FAS mRNA content in the cytosol of rat liver were closely related to the transcriptional activity of FAS gene in the early phase of induction, but another regulatory mechanism seems to operate in the decrease of mRNA after 12 hours.
Animal ; DNA/genetics ; Dietary Carbohydrates/administration & dosage ; Fatty Acid Synthetase Complex/*biosynthesis/genetics ; *Gene Expression Regulation, Enzymologic ; Liver/*enzymology ; Male ; RNA, Messenger/metabolism ; Rats ; Rats, Sprague-Dawley ; *Transcription, Genetic

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

We investigated the change in activity of the sympathetic nervous system (SNS) in high-sucrose diet (HSD)-induced obese rats compared with controls. Power spectral analyses of R-R interval variability were performed to obtain the low frequency (LF, 0.04-0.699 Hz) and high frequency (HF, 0.7-3.0 Hz) powers. The percents of fat mass to body weight (%F/BW) and fat to muscle ratios (F/M) were significantly increased in HSD-fed rats. Plasma glucose, leptin, and triglyceride concentrations in rats fed with HSD were significantly increased. LF in normalized units (LFn), which represents both sympathetic and parasympathetic activities, was significantly increased whereas HF in normalized unit (HFn), which represents parasympathetic activity, was significantly decreased in HSD-fed rats. LF/HF, which represents sympathetic activity, was significantly increased in HSD-fed rats and was correlated with leptin (r=0.549, p<0.023), %F/BW (r=0.513, p<0.035), F/M (r=0.536, p<0.038), and triglyceride (r=0.497, p<0.042). When adjusted for leptin concentrations, however, LF/HF of HSD-fed rats was significantly decreased. In conclusion, HSD-induced obese rats showed increased LF/HF, which was significantly decreased by adjustment for leptin concentrations. We suggest that stimulating effect of leptin on SNS is reduced, which might play a role in induction of obesity by HSD.
Animal ; Body Weight ; Dietary Carbohydrates/administration & dosage ; Disease Models, Animal ; Fats/metabolism ; Male ; Muscles ; Obesity/physiopathology* ; Obesity/metabolism ; Obesity/etiology ; Rats ; Rats, Wistar ; Spectrum Analysis, Mass/methods ; Sympathetic Nervous System/physiopathology*