glycogen and Hypercholesterolemia

3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) are a common and effective treatment for hypercholesterolemia, with a low overall rate of side-effects. The most common complication is some degree of skeletal muscle myopathy, ranging from painless serum creatine kinase elevations to rhabdomyolysis. Unfortunately, the likelihood and/or severity of complications increases with the combination of statin treatment and physical activity. The specific pathways that mediate statin-associated myopathy are unclear, and research directly addressing the exacerbation with exercise is limited. Potential mechanisms include the induction of skeletal muscle fiber apoptosis, alterations in ubiquitin-proteasome pathway activity, mitochondrial dysfunction, and terpenoid depletion. In this review we provide an overview of research that specifically addresses the combination of statin-associated myopathy and physical activity and highlight some deficiencies in the available literature, as well as future directions for this important subset of statin-associated myopathy.

Topics: Creatine Kinase; Exercise; Glycogen; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypercholesterolemia; Muscle, Skeletal; Muscular Diseases; Physical Education and Training; Risk Assessment; Risk Factors

Topics: Animals; Brain Chemistry; Diabetes Mellitus; Diuretics; Glycogen; Hepatolenticular Degeneration; Humans; Hypercholesterolemia; Hyperlipidemias; Liver; Liver Diseases; Poisoning; Skin Diseases; Thioctic Acid

Topics: 3-Hydroxybutyric Acid; Animals; Anticholesteremic Agents; Atherosclerosis; Cholesterol; Diet, High-Fat; Disease Models, Animal; Fatty Acids; Gene Expression Profiling; Gene Expression Regulation, Enzymologic; Glucose; Glucosides; Glycogen; Hypercholesterolemia; Lipidomics; Lipogenesis; Liver; Male; Mice, Inbred C57BL; Mice, Knockout, ApoE; Phenols; Proton Magnetic Resonance Spectroscopy

Background Iodine is a nonpareil constituent of thyroid hormones (THs) and a prime regulator of thyroid gland functioning. Although essential at recommended levels for the prevention of iodine deficiency disorders (IDDs), exposure to excess iodine reportedly causes hypothyroidism, hyperthyroidism, and several other emerging deleterious impacts. The objective of the present study is to explore the influence of excess iodide exposure on carbohydrate and lipid metabolism along with the histoarchitecture of certain associated organs such as the pancreas, liver, kidney, and skeletal and cardiac muscle because information on those aspects was found to be scanty. Methods Twelve rats were taken, six were fed with iodine through gavage at a dose of 3.5 mg potassium iodide (KI)/100-g body weight, which corresponded to 500 times of the physiological daily dosage of iodide for a period of 60 days, while the other six formed the control group. Results KI-treated rats presented high body weight and urinary iodine with low TH levels, suggesting a primary thyroid dysfunction. There was an increase in blood glucose, cholesterol, triglycerides, low density lipoprotein (LDL), and very low density lipoprotein (VLDL), while high density lipoprotein (HDL) levels decreased. Tissue glycogen content in the liver and skeletal muscle was decreased and was increased in the heart and kidney. Histological sections of the pancreas showed a complete disruption with hardly recognizable histoarchistructure. Treated liver sections displayed the broadened central vein with degenerated hepatocytes, while skeletal muscle sections showed dissolution of muscle fibre cells linked with loss of glycogen from these organs. Histological changes in the heart include features similar to those of a fatty heart with cardiac muscles mutilation, while that of the kidney shows an increase in glomerular tuft size and Bowman's space expansion with general deterioration. Conclusions It may thus be concluded that excess iodine exposure for a long duration causes the development of a biochemical state of hypothyroidism. The developed hypothyroidism was found responsible for the hyperglycaemic and hypercholestromic status evident by high blood glucose and cholesterol levels and the depletion of glycogen at its storage sites in the liver and skeletal muscle but the extra deposition in the cardiac muscle and kidney; histomicrophotographs showed severe destruction of the pancreatic structure. All these alterations

Topics: Animals; Blood Glucose; Body Weight; Carbohydrate Metabolism; Drug Overdose; Glycogen; Hypercholesterolemia; Hyperglycemia; Hypothyroidism; Lipid Metabolism; Male; Potassium Iodide; Rats; Rats, Wistar; Thyroid Hormones; Time Factors

High-fat diets and oxidative damage may contribute to the development of type 2 diabetes. Hypolipidaemic drugs and antioxidants were supposed to prevent the development of the disease. In this study, we investigated preventive effects of fenofibrate (200 mg kg(-1)), vitamin C (30 mg kg(-1)), combination of both in mice induced by streptozotocin (35 mg kg(-1)) and soluble lard (15 ml kg(-1)). The results showed the mice demonstrated hyperglycaemia and hypercholesterolaemia, visceral fat accumulation, and a slight increase in liver glycogen/triglyceride and oxidative stress within 60 days of treatment. Fenofibrate enhanced insulin sensitivity, improved glycaemic control, lowered serum triglycerides, reduced body and visceral fat weights, and decreased liver glycogen/lipid levels but showed hepatotoxicity in the mice. Vitamin C neither itself prevented nor enhanced preventive effects of fenofibrate on glucose and lipid metabolism but partly attenuated the hepatotoxicity of fenofibrate. These results suggest that fenofibrate inhibit development of type 2 diabetes induced by high-fat diets and oxidative stress. However, here, vitamin C just can serve as an adjunct to fenofibrate therapy against its hepatotoxicity. In the future study, we should investigate if higher dosage of vitamin C or other antioxidants would enhance preventive effects of fenofibrate in type 2 diabetes.

Topics: Animals; Antioxidants; Ascorbic Acid; Blood Glucose; Chemical and Drug Induced Liver Injury; Cholesterol; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 2; Dietary Fats; Drug Therapy, Combination; Fenofibrate; Glycogen; Hypercholesterolemia; Hyperglycemia; Hypoglycemic Agents; Hypolipidemic Agents; Insulin Resistance; Intra-Abdominal Fat; Liver; Liver Diseases; Male; Matrix Metalloproteinase 9; Mice; Oxidative Stress; Streptozocin; Triglycerides

An investigation was made to reveal the possible involvement of thyroid hormones, if any, in terazosin (an alfa-1 adrenergic receptor blocker) induced alterations in tissue lipid peroxidation (LPO) and in the concentration of different serum lipids. We determined the impact of terazosin on the changes in hypercholesterolemic (CCT) diet induced thyroid dysfunction; cardiac, renal and hepatic LPO and on serum glucose concentration in female Wister rats. Simultaneously levels of total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (TG), creatinine, alkaline phosphatase (ALP) activity, hepatic glycogen synthesis and total daily food consumption were studied as supporting parameters. While a decrease in the level of serum thyroid hormones, HDL-C and in hepatic glycogen content, was observed in CCT diet fed animals; it increased the concentration of other serum lipids, glucose and creatinine; ALP activity; tissue and serum LPO. However, following terazosin administration for 15 days to CCT diet fed animals, status of thyroid hormones and all other thyroid dependent parameters were reversed suggesting that the drug might be acting through an alteration in the thyroid functions.

Topics: Adrenergic alpha-Antagonists; Animals; Blood Glucose; Cholesterol, Dietary; Disease Models, Animal; Eating; Female; Glycogen; Heart; Hypercholesterolemia; Hyperglycemia; Hypoglycemic Agents; Hypolipidemic Agents; Kidney; Lipid Peroxidation; Lipids; Lipoproteins; Liver; Prazosin; Rats; Rats, Wistar; Thyroid Gland; Thyroxine; Triiodothyronine

A considerable amount of clinical and experimental evidence now exists suggesting the involvement of free radical-mediated oxidative processes in the pathogenesis of diabetic complications. If the diabetic state is associated with a generalized increase in oxidative stress, it might well be reflected in the alterations in embryonic and fetal development during pregnancy. In the present study, incidence of the malformed fetuses, biochemical parameters and antioxidant system activity of streptozotocin (STZ)-induced diabetic pregnant rats was investigated and the results obtained were compared with those of the control group (non-diabetic). Virgin female Wistar rats were injected with 40 mg/kg streptozotocin (STZ) before mating. All the females were killed on Day 21 of pregnancy and the fetuses were analyzed. A maternal blood sample was collected by venous puncture and the maternal liver was removed for biochemical measurement. The diabetic dams presented hyperglycemia, hyperlipemia, hypertriglyceridemia, hypercholesterolemia, hyperuricemia, decreased reduced glutathione (GSH), hepatic glycogen and superoxide dismutase (SOD) determinations. There was an increased incidence of skeletal and visceral malformation in fetuses from diabetic rats. Our findings suggest that oxidative stress occurs in the diabetic pregnant state, which might promote maternal homeostasis alterations. These diabetic complications might be a contributory factor to conceptus damage causing embryonic death (abortion/miscarriage) or the appearance of malformations in the fetuses of diabetic dams. Antioxidant treatment of women with diabetes may be important in future attempts to prevent congenital malformations.

Topics: Animals; Antioxidants; Congenital Abnormalities; Diabetes Mellitus, Experimental; Female; Gestational Age; Glutathione; Glycogen; Hypercholesterolemia; Hyperglycemia; Hyperlipidemias; Hypertriglyceridemia; Liver; Male; Oxidative Stress; Pregnancy; Pregnancy in Diabetics; Rats; Rats, Wistar; Superoxide Dismutase; Uric Acid

This feeding trial evaluated the influence of a diet containing heated chickpea in a dietary induced rat model of hypercholesterolemia in order to assess some possible protective and therapeutic effects on lipid and carbohydrate metabolism disorders as found with other legumes. Rats fed a diet enriched with coconut oil (25%) and cholesterol (1%) for 42 days (HH) showed a situation of type IIa hyperlipoproteinemia. However, these lipid alterations were improved in the hypercholesterolemic rats receiving control (HC) and legume (HL) diets for 16 days. Moreover, results confirm that the chickpea was more effective than the control diet containing casein in the normalization of triglycerides as well as total and LDL-cholesterol levels. On the other hand, the HH group showed a marked reduction in the liver glycogen content and Glucose-6-Phase activity (involved in glyconeogenesis) and an increase in Glucokinase (GK) activity (involved in glucose utilization). In contrast, the rats receiving chickpea re-established the liver glycogen deposition as compared to the HH group. Also, the chickpea intake increased the GK activity as compared to the control diet. The overall results support that chickpea intake may be recommended in humans with altered lipid profile such as type IIa hyperlipoproteinemia. Additionally, data concerning carbohydrate utilization indicated its potential positive effects in diabetes therapy and their role as biological active food supplements.

Topics: Animals; Blood Glucose; Cholesterol, Dietary; Cholesterol, HDL; Cholesterol, LDL; Coconut Oil; Fabaceae; Glucokinase; Glucose; Glucosephosphate Dehydrogenase; Glycogen; Hypercholesterolemia; Lipids; Liver; Male; Plant Oils; Plants, Medicinal; Rats; Rats, Wistar; Triglycerides

Topics: Biopsy; Child, Preschool; Epinephrine; Fasting; Fats; Follow-Up Studies; Glucagon; Glucose; Glucosidases; Glycogen; Glycogen Storage Disease; Humans; Hypercholesterolemia; Hyperlipidemias; Infant; Male

Topics: Animals; Cholesterol; Diet, Atherogenic; Epinephrine; Glycogen; Hypercholesterolemia; Male; Phospholipids; Rabbits