33 patients ages of 38-78 in the hospital 175 participated to a study during 1/1998 5/1999. The research found that fenofibrate (lipanthy) at dose of 300 mg per day reduced obviously the total cholesterol, low density lipoprotein cholesterol and triglyceride. The more high level of these, the more effect of the drug was well tolerated and high safety. The side effects were mild and uncommon. The ure, creatinine, transaminase values were not changed by the drug and there were no complication of the gallblader stone
Lipid Metabolism ; Procetofen ; therapeutics

BACKGROUND: To assess the efficacy of fenofibrate treatment in combination with urate lowering agents in patients with gout. METHODS: Fourteen male patients with chronic tophaceous or recurrent acute attacks of gout were evaluated in an open-label pilot study of the hypolipidemic agent, fenofibrate (Lipidil Supra(R) 160 mg/d). Patients were stable on urate lowering agents (allopurinol or benzbromarone) for > or =three months without acute attack for the most recent one month before participating. All patients were being treated with established doses of urate lowering agents without modification throughout the study. Clinical and biochemical assessments including serum uric acid, creatinine, liver function test and fasting serum lipid were measured at (1) baseline (2) after two months of fenofibrate treatment and (3) two months after fenofibrate was withdrawn. RESULTS: Serum uric acid was lowered by 23% after two months of fenofibrate treatment (6.93+/-2.16 vs. 5.22+/-1.16 mg/dL; p=0.016). Triglyceride levels were also reduced after fenofibrate treatment (p=0.001). However, this effect was reversed after the withdrawal (p=0.002) of the drug. Alkaline phosphatase was reduced after fenofibrate treatment (p=0.006), but increased 21% after the withdrawal of the drug (p=0.002). By contrast, serum levels of high density lipoprotein and creatinine were increased 9% (p=0.018) and 12% (p=0.006), respectively; however, both levels were significantly decreased to the baseline levels upon withdrawal of fenofibrate. CONCLUSIONS: Fenofibrate can effectively reduce uric acid levels in addition to its known hypolipidemic effect. Fenofibrate may be used as a potential urate lowering agent in patients with gout, especially in those with coexisting hyperlipidemia.
Uricosuric Agents/*administration & dosage ; Uric Acid/blood ; Procetofen/*administration & dosage ; Middle Aged ; Male ; Lipids/blood ; Humans ; Gout/blood/*drug therapy ; Aged ; Adult

Fenofibrate is a drug that has been suggested to inhibit weight gain by increasing the catabolism of fatty acid in the hepatic mitochondria. We hypothesized that fenofibrate induces an increase in energy expenditure in the hepatic mitochondria, which results in the reduction of adipose tissue. In this study we measured hepatic uncoupling protein (UCP)-2, -3, core temperatures and abdominal fat composition with MRI in Otsuka Long-Evans Tokushima Fatty rats. The fenofibrate group (n=7) was fed fenofibrate (320 mg/kg) mixed chow. The control group (n=7) was fed chow only. The body weight (531.6+/-7.6 g) of the fenofibrate group was significantly lower than that (744.3+/-14.9 g) of the control group (p<0.005). The areas of visceral and subcutaneous fat in the fenofibrate group (11.0+/-0.9 cm2, 4.2+/-0.3 cm2) were significantly less than those in the control group (21.0+/-0.7 cm2, 7.4+/-0.4 cm2) (p=0.046, respectively). The esophageal and rectal temperatures of the fenofibrate group (37.7+/-0.1 degrees C, 33.1+/-0.2 degrees C) were significantly higher than those of the control group (37.3+/-0.1 degrees C, 32.2+/-0.1 degrees C) (p=0.025, p=0.005). There was de novo expression of UCP-3 in the liver of the fenofibrate group. These data suggest that increased energy dissipation, via hepatic UCP-3 by fenofibrate, contribute to decreased weight gain in obese rats.
Rats, Inbred OLETF ; Rats ; Procetofen/*pharmacology ; Obesity/*physiopathology ; Muscle, Skeletal/drug effects/physiopathology ; Liver/drug effects/*physiopathology ; Energy Metabolism/*drug effects ; Body Weight/*drug effects ; Body Temperature/*drug effects ; Antilipemic Agents/administration & dosage ; Animals ; Adipose Tissue/*drug effects

To determine whether the PPARalpha agonist fenofibrate regulates obesity and lipid metabolism with sexual dimorphism, we examined the effects of fenofibrate on body weight, white adipose tissue (WAT) mass, circulating lipids, and the expression of PPARalpha target genes in both sexes of high fat diet-fed C57BL/6J mice. Both sexes of mice fed a high-fat diet for 14 weeks exhibited increases in body weight, visceral WAT mass, as well as serum triglycerides and cholesterol, although these effects were more pronounced among males. Feeding a high fat diet supplemented with fenofibrate (0.05% w/w) reduced all of these effects significantly in males except serum cholesterol level. Females on a fenofibrate-enriched high fat diet had reduced serum triglyceride levels, albeit to a smaller extent compared to males, but did not exhibit decreases in body weight, WAT mass, and serum cholesterol. Fenofibrate treatment resulted in hepatic induction of PPAR alpha target genes encoding enzymes for fatty acid beta-oxidation, the magnitudes of which were much higher in males compared to females, as evidenced by results for acyl-CoA oxidase, a first enzyme of the beta-oxidation system. These results suggest that observed sexually dimorphic effects on body weight, WAT mass and serum lipids by fenofibrate may involve sexually related elements in the differential activation of PPARalpha.
Adipose Tissue/drug effects/metabolism ; Animals ; Body Composition/drug effects ; Body Weight/drug effects ; Diet ; Dietary Fats/pharmacology ; Female ; Gene Expression Regulation/drug effects ; Lipids/blood/*metabolism ; Liver/drug effects/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Obesity/*metabolism/pathology ; Organ Weight/drug effects ; Procetofen/*pharmacology ; Receptors, Cytoplasmic and Nuclear/*agonists ; *Sex Characteristics ; Time Factors ; Transcription Factors/*agonists

Primary hypothyroidism and type 2 diabetes are both typically associated with the increased level of triglycerides. To date, there have been only a few case reports of type 2 diabetes patients with both type V hyperlipoproteinemia and eruptive xanthomas, but there have been no reports of hypothyroidism patients associated with eruptive xanthomas. We report here on a case of a 48-yr old female patient who was diagnosed with type 2 diabetes and primary hypothyroidism associated with both type V hyperlipoproteinemia and eruptive xanthomas. We found rouleaux formation of RBCs in peripheral blood smear, elevated TSH, and low free T4 level, and dyslipidemia (total cholesterol 18.1 mM/L, triglyceride 61.64 mM/L, HDL 3.0 mM/L, and LDL 2.54 mM/L). She has taken fenofibrate, levothyroxine, and oral hypoglycemic agent for 4 months. After treatment, both TSH level and lipid concentration returned to normal range, and her yellowish skin nodules have also disappeared.
Antilipemic Agents/therapeutic use ; Diabetes Mellitus, Type 2/blood/*complications/drug therapy ; Erythrocyte Aggregation ; Female ; Humans ; Hyperlipidemia/blood ; Hyperlipoproteinemia Type V/blood/*complications/drug therapy ; Hypoglycemic Agents/therapeutic use ; Hypothyroidism/blood/*complications/drug therapy ; Middle Aged ; Procetofen/therapeutic use ; Research Support, Non-U.S. Gov't ; Skin Diseases/blood/complications/drug therapy ; Thyrotropin/blood/therapeutic use ; Thyroxine/blood ; Treatment Outcome ; Xanthomatosis/blood/*complications/drug therapy

Peroxisome proliferator-activated receptor alpha (PPARalpha) activation in rodents is thought to improve insulin sensitivity by decreasing ectopic lipids in non-adipose tissues. Fenofibrate, a lipid-modifying agent that acts as a PPARalpha agonist, may prevent adipocyte hypertrophy and insulin resistance by increasing intracellular lipolysis from adipose tissue. Consistent with this hypothesis, fenofibrate decreased visceral fat mass and adipocyte size in high fat diet-fed obese mice, and concomitantly increased the expression of PPARalpha target genes involved in fatty acid beta-oxidation in both epididymal adipose tissue and differentiated 3T3-L1 adipocytes. However, mRNA levels of adipose marker genes, such as leptin and TNFalpha, were decreased in epididymal adipose tissue by fenofibrate treatment. Fenofibrate not only reduced circulating levels of free fatty acids and triglycerides, but also normalized hyperinsulinemia and hyperglycemia in obese mice. Blood glucose levels of fenofibrate-treated mice were significantly reduced during intraperitoneal glucose tolerance test compared with obese controls. These results suggest that fenofibrate-induced fatty acid beta-oxidation in visceral adipose tissue may be one of the major factors leading to decreased adipocyte size and improved insulin sensitivity.
3T3 Cells ; Adipocytes/cytology/*drug effects ; Animals ; Antilipemic Agents/*pharmacology ; Blood Glucose ; Body Weight ; Cell Enlargement/*drug effects ; Dietary Fats ; Gene Expression Regulation/drug effects ; Glucose Tolerance Test ; Insulin/blood ; *Insulin Resistance ; Leptin/genetics ; Lipids/blood ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; PPAR alpha/*metabolism ; Procetofen/*pharmacology ; Tumor Necrosis Factor-alpha/genetics