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

The purpose of the present study was to determine whether chronic high-fat diet (HF) induces insulin resistance independently of obesity. We randomly divided 40 rats into two groups and fed them either with a HF or with a high-carbohydrate diet (HC) for 8 weeks. Whole body glucose disappearance rate (Rd) was measured using a euglycemic hyperinsulinemic clamp. Firstly, we defined whether insulin resistance by HF was associated with obesity. Plasma glucose and triglyceride concentrations were significantly increased in HF. Rd was decreased (10.6+/-0.2 vs. 9.1+/-0.2 mg/kg/min in HC and HF, respectively) and the hepatic glucose output rate (HGO) was increased in HF (2.2+/-0.3 vs. 4.5+/-0.2 mg/kg/min in HC and HF, respectively). Rd was significantly correlated with %VF (p<0.01). These results implicate that visceral obesity is associated with insulin resistance induced by HF. In addition, to define whether dietary fat induces insulin resistance regardless of visceral obesity, we compared Rd and HGO between groups 1) after matching %VF in both groups and 2) using an ANCOVA to adjust for %VF. After matching %VF, Rd in HF was significantly decreased by 14% (p<0.001) and HGO was significantly increased by 110% (p<0.001). Furthermore, statistical analyses using an ANCOVA also showed Rd for HF was significantly decreased even after adjusting %VF. In conclusion, we suggest that dietary fat per se could induce insulin resistance in rats fed with chronic HF independently of obesity.
Adipose Tissue/*pathology ; Animal ; Dietary Carbohydrates/administration &age ; Dietary Fats/*administration &age ; Fatty Acids, Nonesterified/metabolism ; Female ; *Insulin Resistance ; Obesity/etiology ; Rats ; Rats, Sprague-Dawley ; Viscera

OBJECTIVETo study the mechanism of the effect of low-frequency rotary constant magnetic field on high-fat and high-protein diet-induced fatty liver in rats.

METHODSFatty liver model was established in SD rats by feeding on a high-fat and high-protein diet daily. The enzyme activity changes in the serum and liver homogenate were detected at 10, 14, and 18 weeks, and the pathological changes of the liver were observed with optical and electron microscopy.

RESULTSIn magnetic field intervention group, the concentration of alanine aminotransferase and aspartate transaminase were significantly decreased, and the activity of lipoprotein lipase, hepatic lipase, superoxide dismutase and the concentration of malondialdehyde in the liver homogenate were significantly increased. Under optical microscope and electron microscope, the rats in the model group showed diffusive adipose degeneration in the hepatic cells with large lipid droplets, which became large vacuoles after fat extraction, indicating fatty necrosis. In magnetic field intervention group, remarkably smaller lipid droplets and lessened hepatic cell adipose degeneration were observed.

CONCLUSIONLow-frequency rotary constant magnetic field has beneficial effect on fat metabolism, leading to reduced lipid peroxidation and structural recovery of the degenerated hepatic cells.

Animals ; Dietary Fats ; administration & dosage ; Dietary Proteins ; administration & dosage ; Fatty Liver ; etiology ; pathology ; therapy ; Magnetic Field Therapy ; Male ; Random Allocation ; Rats ; Rats, Sprague-Dawley

We examined the effects of conjugated linoleic acid (CLA) on growth, fatty acid composition and enzyme activity of fatty acid oxidation in the liver of large yellow croaker. We divided 1600 fish (average initial weight 150 g) into 4 groups and reared them in 8 cages. Four dietary treatments were formulated to contain 0%, 1%, 2% and 4% (w/w) CLA, respectively. The fish were fed for 10 weeks ad libitum twice daily. We found that the dietary CLA had no effect on growth, biometric parameters and whole body proximate (P>0.05), but showed some significant effects on the fatty acid composition in both muscle and the liver. The activities of lipogenic enzymes were slightly depressed in fish fed with increasing levels of CLA when compared with control (P>0.05). Dietary CLA supplementation had no effects on liver lipid content, but significantly increased the contents of saturated fatty acids (SFA) and polyunsaturated fatty acids (PUFA) (P<0.05) and decreased monounsaturated fatty acid (MUFA) content in both muscle and the liver. Dietary CLA inclusion resulted in significant increases of the biologically active cis-9, trans-11 and trans-10, cis-12 isomers in both tissues (P<0.05). The total accumulation of CLA was higher in the liver (3.83%, w/w) than in muscle (3.77%, w/w) when fed with 4% (w/w) CLA. This study demonstrates that large yellow croakers are capable of absorbing and depositing CLA and long-chain n-3 PUFA in the liver and muscle, showing that this species fed with CLA could be an important human food source for these healthful fatty acids.
Animals ; Dietary Fats ; administration & dosage ; Dietary Supplements ; Fatty Acids ; metabolism ; Linoleic Acid ; administration & dosage ; Lipogenesis ; drug effects ; physiology ; Liver ; drug effects ; metabolism ; Perciformes ; growth & development ; metabolism

OBJECTIVETo create a rat insulin resistant fatty liver model.

METHODS14 male Wistar rats were randomly divided into a model and a control group. The model rats were fed a high-fat diet (45% of energy from fat) for 8 weeks, and the control group a standard diet (19% of energy from fat). Insulin sensitivity was measured with glucose infusion rate (GIR) by the euglycermic hyperinsulinemia clamp technique. The aminotransferase, triglyceride (TG), free fatty acid (FFA), superoxide dismutase (SOD) and malondialdehyde (MDA) were measured by biochemical methods, and insulin was measured by radioimmunoassay. The histological and ultrastructural changes of all rat livers were scored using light and electron microscopy.

RESULTSRats fed the high-fat diet developed panlobular macrovesicular steatosis, lobular inflammatory cell infiltration and abnormal mitochondria, whereas those fed the standard diet had normal livers. All model group rats had elevated levels of aminotransferase, TG, FFA, insulin and liver index, and low GIR. In addition, the high-fat diet increased MDA and decreased SOD.

CONCLUSIONA fatty liver and insulin resistance model was successfully developed in rats fed a high-fat diet for 8 weeks, which provided a useful experimental tool for elucidating pathogenesis and treatment of fatty liver.

Animals ; Dietary Fats ; administration & dosage ; Disease Models, Animal ; Fatty Liver ; metabolism ; physiopathology ; Insulin Resistance ; Male ; Random Allocation ; Rats ; Rats, Wistar

OBJECTIVETo explore the influence of acute glucose and fat loading on endothelium dependent flow-mediated vasodilation (FMD) in patients with essential hypertension (EH).

METHODSPatients with EH were randomly divided into three groups: oral glucose loading alone (n = 26), oral standardized fat loading alone (n = 38), combined glucose and fat loading (n = 34). FMD of the brachial artery was assessed by high resolution ultrasound technique respectively.

RESULTS(1) Compared to control group, postprandial abnormal serum triglyceride metabolism was evidenced and FMD was significantly reduced and the lowest FMD occurred at 4 hours and returned to the baseline level at 8 hours post fat loading alone in EH patients. (2) GS-AUC and 1 hour glucose were significantly higher in EH patients than in controls (all P < 0.05), FMD was also significant decreased (-31.4%) at 1 hour and returned to baseline level at 2 hours post oral glucose loading. (3) After combined glucose and fat loading, FMD at 1 hour (5.45 ± 1.93 vs. 9.46 ± 3.33, P < 0.05) was significantly lower than that in glucose loading alone and FMD at 4 hours (7.98 ± 1.64 vs. 9.66 ± 2.26, P < 0.05), was also lower than that in fat loading alone in EH patients. (4) FMD was negatively correlated with SBP, GS-AUC, DBP, TG-AUC (γ = -0.46, -0.44, -0.41, -0.38, respectively, all P < 0.05).

CONCLUSIONCombined glucose and fat loading additively reduced FMD in hypertensive patients.

Adult ; Aged ; Brachial Artery ; physiopathology ; Dietary Fats ; administration & dosage ; Endothelium, Vascular ; physiopathology ; Female ; Glucose ; administration & dosage ; Humans ; Hypertension ; physiopathology ; Male ; Middle Aged ; Triglycerides ; blood ; Vasodilation

OBJECTIVEto explore the value of in vivo dynamic monitoring of abdominal aortic atherosclerosis (AS) by high field magnetic resonance (MR) imaging (MRI) in apoE-/- mice fed a high fat diet or infused with angiotensin.

METHODShigh fat diet or angiotensin II infusion was applied to apoE-/- mice for establishment of abdominal aortic atherosclerosis model. Abdominal aorta MRI was performed at 3 time points (baseline, 3 and 6 months) in 13 high fat diet fed apoE-/- mice aged 10-12 months and 3 wild-type control mice; 10 apoE-/- mice aged 6 months were infused with angiotensin II (1000 or 500 ng × kg(-1)× min(-1), n = 5 each) or saline for 14 d through Osmotic minipump. The abdominal aortic artery MRI was performed at baseline and 14 d after infusion. Black blood sequences of FLASH T1 weighted images and Proton density weighted-T2 weighted dual echo images were obtained. At each observation time post MRI, mice (n = 3, 5 and 5 for high fat diet group and n = 5 and 5 for angiotensin II infusion group) were sacrificed for pathological examination of the abdominal artery.

RESULTS(1) the abdominal aorta atherosclerosis was identified in both high fat diet and angiotensin II treated apoE-/- mice but in WT controls. Lesion progression was documented in high fat diet fed apoE-/- mice characterized by significantly increased vessel wall (a marker of atherosclerotic burden, F = 29.94, P < 0.05) and gradually increased plaque signal in PDW and T2W images. Results derived from MRI corresponded histopathology findings in high fat diet fed apoE-/- mice (correlative coefficient = 0.84, 0.95, 0.90, P < 0.05, respectively). Both MRI and histology showed increased lipid composition and decreased fibrotic composition in these mice. (2) The vessel wall area increased significantly [(1.21 ± 0.21) mm(2) vs. (2.65 ± 0.48) mm(2), P < 0.05] and the abdominal aortic dissection aneurysms was identified in apoE-/- mice infused with high angiotensin II. The vessel wall area also increased [(0.85 ± 0.11) mm(2) vs. (1.01 ± 0.17) mm(2), P < 0.05] in low angiotensin II infused apoE-/- mice and the coefficient between MR and histopathology is 0.934.

CONCLUSIONabdominal aortic unstable plaque model could be established by both high fat diet and angiotensin II infusion in apoE mice, angiotensin II infusion can transiently accelerate the progression of AS and can induce abdominal aortic dissection. Serial MR black blood sequences could demonstrate the development and progression of atherosclerosis in mouse abdominal aorta with excellent agreement to histopathology finding in terms of atherosclerotic burden and plaque composition. Thus, MRI appears to be a useful tool for in vivo AS plaque dynamic monitoring in mice.

Angiotensin II ; administration & dosage ; Animals ; Aorta, Abdominal ; Apolipoproteins E ; Arteriosclerosis ; Diet ; Dietary Fats ; administration & dosage ; Disease Models, Animal ; Magnetic Resonance Imaging ; methods ; Male ; Mice ; Mice, Knockout

The present study was designed to investigate the effects of high-saturated and high-unsaturated fatty acid diets on relaxation and contraction of the renal arteries in insulin resistance (IR) rats. Wistar rats were fed normal chow diet (control), high-saturated fatty acid diet or high-unsaturated fatty acid diet for 6 months (n=14 in each group). IR was evaluated by glucose infusion rate (GIR) of hyperinsulinemic euglycemic clamp. Blood pressure was measured via the tail-cuff method. Body weight (BW), plasma total triglyceride (TG), free fatty acid (FFA), insulin, fasting blood glucose (FBG) and nitric oxide metabolite (NO2(-)/NO3(-)) were compared among the three groups. The rats were sacrificed and the renal arterial rings were placed in the physiological tissue baths for measurement of vascular response to various agents. After the arterial rings were constricted with 3 mmol/L noradrenaline (NA), endothelium-dependent vasorelaxation to acetylcholine (ACh) and endothelium-independent vasorelaxation to sodium nitroprusside (NTP) were measured. Endothelium-dependent vasorelaxation to ACh was also observed in renal arterial rings incubated with L-arginine (L-Arg), N(omega)-nitro-L-arginine (L-NNA) and methylene blue (MB), respectively. Arterial contractility was evaluated from concentration-response curves to 10 nmol/L-100 micromol/L NA. Saturated or unsaturated fatty acids led to moderate rises in blood pressure (P<0.05). It was associated with higher levels of plasma lipids and lower whole body insulin sensitivity (P<0.01). There were no significant differences in BW, FBG, TG, insulin and FFA between saturated and unsaturated fatty acid-fed rats. A decrease in endothelium-dependent vasorelaxation of the renal arteries in saturated and unsaturated fatty acid-fed rats was observed (P<0.01), but there was no marked difference between the two high-fatty acid diet groups. Endothelium-dependent vasorelaxation was increased when the arteries were incubated with L-Arg and decreased when incubated with L-NNA and MB in both high-fatty acid diet groups (P<0.05, P<0.01). But no difference was found before and after incubation with L-Arg, L-NNA and MB in the control rats. In the mean time, endothelium-independent maximal vasorelaxation response of renal arteries to NTP and renal arterial contractile responses to cumulative dose of NA were assayed, and there was no difference among the three groups (P>0.05). Endothelium-dependent vasorelaxation was negatively correlated with systolic blood pressure and TG, and positively correlated with NO2(-)/NO3(-) and GIR. There was a significantly negative correlation between FFA and NO2(-)/NO3(-). The present study suggests that both high-saturated and unsaturated fatty acid diets result in hypertension associated with significantly decreased endothelium-dependent vasorelaxation, dyslipidemia and IR, and that decreased endothelium-dependent vasorelaxation induced by high fatty acid diets is associated with impaired L-Arg-NO-cGMP pathways.
Animals ; Dietary Fats, Unsaturated ; administration & dosage ; Endothelium, Vascular ; physiology ; Fatty Acids ; administration & dosage ; Insulin Resistance ; Male ; Nitric Oxide ; physiology ; Rats ; Rats, Wistar ; Renal Artery ; physiology ; Systole ; Vasoconstriction ; Vasodilation

OBJECTIVETo survey the intake of dietary lipids and analyze serum lipid levels in hypertensive patients, and to study the effects of changing dietary lipids intake on the serum lipid levels.

METHODSTo estimate the intake of dietary fat and to measure the level of serum lipids in hypertensive patients before and after intervention.

RESULTSThe baseline survey showed that the intake of dietary fat and cholesterol were high in those patients. Their fat intake is more than 30% of the total energy intake; serum total cholesterol (TC), triglycerides (TG) and LDL-cholesterol (LDL-C) levels were higher than the normal level. Correlation analysis showed that body mass index (BMI) and saturated fatty acid (SFA) intake were positively correlated with serum TC, TG and LDL-C; serum HDL-C/TC ratio was positively correlated with monounsaturated fatty acid (MUFA) intake, and negatively correlated with BMI and SFA. The results implicated that MUFA is the protective factor against hypertension and hyperlipidemia. After one-year community-based nutrition intervention, the serum TC and LDL-C levels of the intervened subjects were reduced dramatically.

CONCLUSIONThe results indicate that reducing the intake of dietary fat and cholesterol and properly increasing dietary MUFA intake have significant effects on lowering serum lipids levels and controlling blood pressure in hypertensive patients.

Aged ; Blood Pressure ; drug effects ; Body Mass Index ; Cholesterol ; blood ; Cholesterol, Dietary ; administration & dosage ; Cholesterol, LDL ; blood ; Dietary Fats ; administration & dosage ; Fatty Acids, Monounsaturated ; administration & dosage ; Female ; Humans ; Hypertension ; blood ; physiopathology ; Lipids ; blood ; Male ; Middle Aged ; 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