ABSTRACT
Lipids play many structural and metabolic roles, and dietary fat has great impact on metabolism and health. Fatty acid oxidation rate is dependent on tissue types. However there has been no report on the relationship between the rate of fatty acid oxidation and carnitine transport system in outer mitochondrial membrane of many tissues. In this study, the rate of fatty acid oxidation and carnitine palmitoyltransferase (CPT) I activity in the carnitine transport system were measured to understand the metabolic characteristics of fatty acid in various tissues. Palmitic acid oxidation rate and CPT I activity in various tissues were measured. Tissues were obtained from the white and red skeletal muscles, heart, liver, kidney and brain of rats. The highest lipid oxidation rate was demonstrated in the cardiac muscle, and the lowest oxidation rate was in brain. Red gastrocnemius muscle followed to the cardiac muscle. Lipid oxidation rates of kidney, white gastrocnemius muscle and liver were similar, ranging from 101 to 126 DPM/mg/hr. CPT I activity in the cardiac muscle was the highest, red gastrocnemius muscle followed by liver. Brain tissue showed the lowest CPT I activity as well as lipid oxidation rate, although the values were not significantly different from those of kidney and white gastrocnemius muscle. Therefore, lipid oxidation rate was highly (p< 0.001) related to CPT I activity. Lipid oxidation rate is variable, depending on tissue types, and is highly (p< 0.001) related to CPT I activity. CPT I activity may be a good marker to indicate lipid oxidation capacity in various tissues.
Subject(s)
Animals , Rats , Brain , Carnitine O-Palmitoyltransferase , Carnitine , Dietary Fats , Heart , Kidney , Liver , Metabolism , Mitochondrial Membranes , Muscle, Skeletal , Myocardium , Palmitic Acid , TransferasesABSTRACT
BACKGROUND: The treatment of rheumatoid arthritis still depend on conserve therapy in major. Recent studies report that n-3 polyunsaturated fatty acids(PUFA) could modulate the incidence and progress of arthritis. The purpose of this study was to investigate the effects of n-3 PUFA on the development of collagen-induced arthritis in rats. MATERIALS AND METHODS: Female Louvain rats were used for this experiment. Rats were randomly assigned into either normal(n=8) or collagen-immunized groups, and collagen immunized groups were divided into control(n=8, normal diet) and n-3 PUFA(n=8, 5% n-3 PUFA in diet) groups. One week after feeding n-3 PUFA to rats, they were immunized with type II collagen emulsified in incomplete Freund's adjuvant into tail and back. Development of arthritis was confirmed by x-ray and microscopic examination. RESULTS: Incidence of arthritis at the 5th week after immunization was 38% in control and 0% in n-3 PUFA. Rats with arthritis showed edema in hind paws and inflammation in synovial membrane of the knee joint. Plasma glucose and insulin were not changed by both of immunization and diet. Plasma triglycerides and cholesterol concentrations were decreased by n-3 PUFA. CONCLUSION: n-3 PUFA may prevent or treat collagen-induced arthritis in rats. Further studies are needed for action mechanism of it.
Subject(s)
Animals , Female , Humans , Rats , Arthritis , Arthritis, Experimental , Arthritis, Rheumatoid , Blood Glucose , Cholesterol , Collagen , Collagen Type II , Diet , Edema , Fatty Acids, Omega-3 , Freund's Adjuvant , Immunization , Incidence , Inflammation , Insulin , Knee Joint , Plasma , Synovial Membrane , Tail , TriglyceridesABSTRACT
BACKGROUND: The treatment of rheumatoid arthritis still depend on conserve therapy in major. Recent studies report that n-3 polyunsaturated fatty acids(PUFA) could modulate the incidence and progress of arthritis. The purpose of this study was to investigate the effects of n-3 PUFA on the development of collagen-induced arthritis in rats. MATERIALS AND METHODS: Female Louvain rats were used for this experiment. Rats were randomly assigned into either normal(n=8) or collagen-immunized groups, and collagen immunized groups were divided into control(n=8, normal diet) and n-3 PUFA(n=8, 5% n-3 PUFA in diet) groups. One week after feeding n-3 PUFA to rats, they were immunized with type II collagen emulsified in incomplete Freund's adjuvant into tail and back. Development of arthritis was confirmed by x-ray and microscopic examination. RESULTS: Incidence of arthritis at the 5th week after immunization was 38% in control and 0% in n-3 PUFA. Rats with arthritis showed edema in hind paws and inflammation in synovial membrane of the knee joint. Plasma glucose and insulin were not changed by both of immunization and diet. Plasma triglycerides and cholesterol concentrations were decreased by n-3 PUFA. CONCLUSION: n-3 PUFA may prevent or treat collagen-induced arthritis in rats. Further studies are needed for action mechanism of it.
Subject(s)
Animals , Female , Humans , Rats , Arthritis , Arthritis, Experimental , Arthritis, Rheumatoid , Blood Glucose , Cholesterol , Collagen , Collagen Type II , Diet , Edema , Fatty Acids, Omega-3 , Freund's Adjuvant , Immunization , Incidence , Inflammation , Insulin , Knee Joint , Plasma , Synovial Membrane , Tail , TriglyceridesABSTRACT
BACKGROUND: It is doubtful that aging causes deteriorated glucose metabolism and insulin resistance of skeletal muscle. Some researchers had different results about it. So we have studied the mechanism responsible for the abnormal glucose tolerance associated with aging in rapidly growing and matured rats. MATERIALS AND METHODS: Animals were used S.D. rats. Growing rats were 7 weeks old (BW: 160-190 gm) and matured rats were 28 weeks old (BW: 420-525 gm). RESULTS: Fasting blood glucose and plasma insulin levels were significantly elevated in matured rat compared with growing rats. And during oral glucose tolerance test the glucose level was also significantly elevated in matured rats. These results confirmed an insulin resistant state of aging. Insulin levels at 30 minutes of oral glucose tolerance test was significantly elevated in growing rat. But at 120 minutes it was maintained at higher level in matured rats than in growing rats. It suggested the possibility of increased insulin secretion by initial stimulation of beta-cells in growing rats, and increased secretion and decreased catabolic rate of insulin in matured rats. Glucose uptake rate of soleus muscle in matured rats was lower than that of growing rats, but the difference was not statistically significant. The dose(insulin)- responsive (glucose uptake) curve of soleus muscle was only slightly deviated to the right side. CONCLUSION: Glucose metabolism of rat skeletal muscle was worsened by aging. The data of glucose uptake experiments suggested the possibility of insulin resistance of skeletal muscle in matured rats, but the mechanism of insulin resistance of skeletal muscle need further studies.
Subject(s)
Animals , Rats , Aging , Blood Glucose , Fasting , Glucose Tolerance Test , Glucose , Insulin , Insulin Resistance , Metabolism , Muscle, Skeletal , PlasmaABSTRACT
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.
Subject(s)
Female , Rats , Adipose Tissue/pathology , Animals , Dietary Carbohydrates , Dietary Fats , Fatty Acids, Nonesterified/metabolism , Insulin Resistance , Obesity/etiology , Rats, Sprague-Dawley , VisceraABSTRACT
The purpose of the present study was to determine the preventive effects of combined interventional trial of fish oil treatment and exercise training on insulin resistance of skeletal muscle in high-fat fed rats. Male Wistar rats were randomly divided into chow diet (CD), high-fat diet (HF), high-fat diet with fish oil (FO), high-fat diet with exercise training (EX), and FO+EX groups. The rats in control group were fed chow diet containing, as percents of calories, 58.9% carbohydrate, 12.4% fat, and 28.7% protein. High-fat diet provided 32% energy as lard, 18% as corn oil, 27% as carbohydrate and 23% as casein. The fish oil diet had the same composition as the high fat diet except that 100 g menhaden oil was substituted for corn oil. Insulin sensitivity was assessed by in vitro glucose transport in the soleus muscle after diet treatment and treadmill running for 4 weeks. While the FO or EX only partially prevented insulin resistance on glucose transport and visceral obesity induced by high-fat diet, these interventions completely corrected hyperinsulinemia and hyperglycemia from the high-fat diet. The rats in the FO+EX showed normalized insulin action on glucose transport, plasma chemicals and visceral fat mass. Insulin-mediated glucose transport was negatively associated with total visceral fat mass (r=-0.734; p<0.000), plasma triglyceride (r=-0.403; p<0.05) and lepin (r=-0.583; p<0.001) concentrations with significance. Multiple stepwise regression analysis showed that only total visceral fat mass was independently associated with insulin-mediated glucose transport (r=-0.668; p<0.000). In conclusion, combined interventional trial of FO+EX recovered insulin resistance on glucose transport of skeletal muscle induced by high-fat diet. Visceral fat mass might be more important factor than plasma TG and leptin to induce insulin resistance on glucose transport of skeletal muscle in high-fat fed rats.
Subject(s)
Animals , Humans , Male , Rats , Caseins , Corn Oil , Diet , Diet, High-Fat , Glucose , Hyperglycemia , Hyperinsulinism , Insulin Resistance , Insulin , Intra-Abdominal Fat , Leptin , Muscle, Skeletal , Obesity, Abdominal , Plasma , Rats, Wistar , Running , TriglyceridesABSTRACT
To investigate whether BCG, lymphtoxin (LT) or bee venom (BV) can prevent insulitis and development of diabetes in non-obese diabetic (NOD) mice, we measured the degree of insulitis and incidence of diabetes in 24 ICR and 96 female NOD mice. NOD mice were randomly assigned to control, BCG-, LT-, and BV-treated groups. The BCG was given once at 6 weeks of age, and LT was given in 3 weekly doses from the age of 4 to 10 weeks. The BV was injected in 2 weekly doses from the age of 4 to 10 weeks. Diabetes started in control group at 18 weeks of age, in BCG group at 24 weeks of age, and in LT- or BV-treated group at 23 weeks of age. Cumulative incidences of diabetes at 25 weeks of age in control, BCG-, LT-, and BV-treated NOD mice are 58, 17, 25, and 21%, respectively. Incidence and severity of insulitis were reduced by BCG, LT and BV treatment. In conclusion, these results suggest that BCG, LT or BV treatment in NOD mice at early age inhibit insulitis, onset and cumulative incidence of diabetes.