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Beneficial Effects of Exercise Training (Treadmill) on Body Mass and Skeletal Muscle Capillaries/Myocyte Ratio in C57BL/6 Mice Fed High-Fat Diet
Motta,Victor Faria; Mandarim de Lacerda,Carlos Alberto;
International Journal of Morphology , 2012, DOI: 10.4067/S0717-95022012000100037
Abstract: c57bl/6 mice develop signals and symptoms comparable at least in part with the metabolic syndrome in humans. this study aimed to evaluate the beneficial effects of exercise training upon skeletal microcirculation in these mice. animals were fed one of two diets during an eight week period: standard chow (sc) or very high-fat (hf). afterwards, the exercise training protocol (treadmill) was established and mice divided into sc and hf sedentary (sc-sed, hf-sed) or exercised groups (sc-ex, hf-ex), respectively. hf/hf-sed mice had the greatest body mass (plus 65% than sc-sed; p<0.0001), and exercise reduced it by 23% (p<0.0001). the plasma insulin was higher in the hf-sed than in the matched -ex (p<0.001). the ratio between capillaries/myocytes in hf-ex group increased by 64% than in hf-sed group (p<0.001) and increased by 80% in sc-ex group than in sc-sed group (p<0.001). in conclusion, exercise improved the lipid profile by reducing body mass gain, insulin resistance, ameliorating the skeletal muscle microcirculation.
Beneficial Effects of Exercise Training (Treadmill) on Body Mass and Skeletal Muscle Capillaries/Myocyte Ratio in C57BL/6 Mice Fed High-Fat Diet Efectos Beneficiosos del Ejercicio Físico (Cinta) sobre la Masa Corporal y Relación Capilares/Miocito del Músculo Esquelético en Ratones C57BL/6 Alimentados con una Dieta Alta en Grasas
Victor Faria Motta,Carlos Alberto Mandarim de Lacerda
International Journal of Morphology , 2012,
Abstract: C57BL/6 mice develop signals and symptoms comparable at least in part with the metabolic syndrome in humans. This study aimed to evaluate the beneficial effects of exercise training upon skeletal microcirculation in these mice. Animals were fed one of two diets during an eight week period: standard chow (SC) or very high-fat (HF). Afterwards, the exercise training protocol (treadmill) was established and mice divided into SC and HF sedentary (SC-Sed, HF-Sed) or exercised groups (SC-Ex, HF-Ex), respectively. HF/HF-Sed mice had the greatest body mass (plus 65% than SC-Sed; P<0.0001), and exercise reduced it by 23% (P<0.0001). The plasma insulin was higher in the HF-Sed than in the matched -Ex (P<0.001). The ratio between capillaries/myocytes in HF-Ex group increased by 64% than in HF-Sed group (P<0.001) and increased by 80% in SC-Ex group than in SC-Sed group (P<0.001). In conclusion, exercise improved the lipid profile by reducing body mass gain, insulin resistance, ameliorating the skeletal muscle microcirculation. Los ratones C57BL/6 desarrollan se ales y síntomas similares al menos en parte con el síndrome metabólico en los seres humanos. Este estudio tuvo como objetivo evaluar los efectos beneficiosos del ejercicio físico sobre la microcirculación ósea en estos ratones. Los animales fueron alimentados con una de dos dietas durante un período de ocho semanas: comida estándar (CE) o muy alta en grasas (AG). Posteriormente, fue establecido un protocolo de entrenamiento físico (cinta) y los ratones fueron divididos en grupos CE y AG sedentarios (CE-Sed, AG-Sed) o grupos de ejercicios (CE-Ej, AG-Ej), respectivamente. Los ratones AG/AG-SED tuvieron una masa corporal mayor (más del 65% de CE-Sed, p <0,0001), y el ejercicio se redujo en un 23% (p <0,0001). La insulina en el plasma fue mayor en el AG-Sed que en el pareado-Ej (p <0,001). La relación entre capilares/miocitos en el grupo AG-Ej aumentó en un 64% más que en el grupo AG-Sed (p <0,001) y aumentó en un 80% más en el grupo CE-Ej que en el grupo CE-Sed (p <0,001). En conclusión, el ejercicio mejora el perfil lipídico mediante la reducción de la ganancia de masa corporal, resistencia a la insulina, mejorando la microcirculación del músculo esquelético.
Evaluation of Beneficial Metabolic Effects of Berries in High-Fat Fed C57BL/6J Mice  [PDF]
Lovisa Heyman,Ulrika Axling,Narda Blanco,Olov Sterner,Cecilia Holm,Karin Berger
Journal of Nutrition and Metabolism , 2014, DOI: 10.1155/2014/403041
Abstract: Objective. The aim of the study was to screen eight species of berries for their ability to prevent obesity and metabolic abnormalities associated with type 2 diabetes. Methods. C57BL/6J mice were assigned the following diets for 13 weeks: low-fat diet, high-fat diet or high-fat diet supplemented (20%) with lingonberry, blackcurrant, bilberry, raspberry, a?ai, crowberry, prune or blackberry. Results. The groups receiving a high-fat diet supplemented with lingonberries, blackcurrants, raspberries or bilberries gained less weight and had lower fasting insulin levels than the control group receiving high-fat diet without berries. Lingonberries, and also blackcurrants and bilberries, significantly decreased body fat content, hepatic lipid accumulation, and plasma levels of the inflammatory marker PAI-1, as well as mediated positive effects on glucose homeostasis. The group receiving a?ai displayed increased weight gain and developed large, steatotic livers. Quercetin glycosides were detected in the lingonberry and the blackcurrant diets. Conclusion. Lingonberries were shown to fully or partially prevent the detrimental metabolic effects induced by high-fat diet. Blackcurrants and bilberries had similar properties, but to a lower degree. We propose that the beneficial metabolic effects of lingonberries could be useful in preventing obesity and related disorders. 1. Introduction During the last decades, the prevalence of obesity and type 2 diabetes mellitus has increased dramatically. This epidemic of lifestyle-related disorders is affecting all parts of the world, and 439 million people are estimated to suffer from diabetes mellitus in 2030 [1]. Obesity is a strong risk factor for type 2 diabetes with 90% of affected patients being overweight or obese. Obesity is also associated with increased risk of various metabolic disorders including insulin resistance, chronic low-grade inflammation, dyslipidemia, nonalcoholic fatty liver disease (NAFLD), and cardiovascular disease. Oxidative stress, inflammatory response, and altered gut microbiota can play a significant role in the development of obesity-related disorders [2–4]. Type 2 diabetes is a multifactorial disease; however, it appears clear that prevention is possible by avoiding overeating and a sedentary lifestyle to maintain a healthy body weight [5]. The difficulty for many individuals to comply with dietary and lifestyle changes makes it of great interest to identify new foods with well-established effects on preventing the development of obesity and thereby type 2 diabetes and its associated metabolic
Metformin Prevents and Reverses Inflammation in a Non-Diabetic Mouse Model of Nonalcoholic Steatohepatitis  [PDF]
Yuki Kita, Toshinari Takamura, Hirofumi Misu, Tsuguhito Ota, Seiichiro Kurita, Yumie Takeshita, Masafumi Uno, Naoto Matsuzawa-Nagata, Ken-ichiro Kato, Hitoshi Ando, Akio Fujimura, Koji Hayashi, Toru Kimura, Yinhua Ni, Toshiki Otoda, Ken-ichi Miyamoto, Yoh Zen, Yasuni Nakanuma, Shuichi Kaneko
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0043056
Abstract: Background Optimal treatment for nonalcoholic steatohepatitis (NASH) has not yet been established, particularly for individuals without diabetes. We examined the effects of metformin, commonly used to treat patients with type 2 diabetes, on liver pathology in a non-diabetic NASH mouse model. Methodology/Principal Findings Eight-week-old C57BL/6 mice were fed a methionine- and choline-deficient plus high fat (MCD+HF) diet with or without 0.1% metformin for 8 weeks. Co-administration of metformin significantly decreased fasting plasma glucose levels, but did not affect glucose tolerance or peripheral insulin sensitivity. Metformin ameliorated MCD+HF diet-induced hepatic steatosis, inflammation, and fibrosis. Furthermore, metformin significantly reversed hepatic steatosis and inflammation when administered after the development of experimental NASH. Conclusions/Significance These histological changes were accompanied by reduced hepatic triglyceride content, suppressed hepatic stellate cell activation, and the downregulation of genes involved in fatty acid metabolism, inflammation, and fibrogenesis. Metformin prevented and reversed steatosis and inflammation of NASH in an experimental non-diabetic model without affecting peripheral insulin resistance.
Liver fatty acid composition in mice with or without nonalcoholic fatty liver disease
Xin Wang, Yuzhen Cao, Yunwei Fu, Guifang Guo, Xiuying Zhang
Lipids in Health and Disease , 2011, DOI: 10.1186/1476-511x-10-234
Abstract: A pathological examination found that NAFLD had developed in the C57BL/6J mice. High-fat feed and CCl4 led to significant increases in C14:0, C16:0, C18:0 and C20:3 (P < 0.01), and decreases in C15:0, C18:1, C18:2 and C18:3 (P < 0.01) in the mouse liver. The treatment also led to an increase in SFA and decreases in other fatty acids (UFA, PUFA and MUFA). An increase in the ratio of product/precursor n-6 (C20:4/C18:2) and n-3 ([C20:5+C22:6]/C18:3) and a decrease in the ratio of n-6/n-3 (C20:4/[C20:5+C22:6]) were also observed.These data are consistent with the hypothesis that fatty acids are deranged in mice with non-alcoholic fatty liver injury induced by high-fat feed and CCl4, which may be involved in its pathogenesis and/or progression via an unclear mechanism.Nonalcoholic fatty liver disease (NAFLD) encompasses a spectrum of conditions that are histologically characterized by hepatic steatosis in individuals without significant alcohol consumption and with no viral, congenital, or autoimmune liver disease markers [1]. It is associated with insulin resistance and metabolic syndrome [2,3]. Despite the many possible etiologies of NAFLD [4,5], these results reflect the accumulation of lipids within the hepatocyte cytoplasm.High-fat feed ingestion and hepatic toxins (such as CCl4) may lead to fatty acid accumulation and hepatic damage. Hepatic lipid accumulation in hepatocytes (hepatic steatosis) is the hallmark of NAFLD and an important factor that can induce insulin resistance, lipid peroxidation, changes in energy metabolism, hepatic cell damage and inflammation. Fatty acid are the simplest lipids. They are the basic components of more complex lipids (including triglycerides, phospholipids and sphingolipids) and an important metabolic fuel. The compositions of the lipids that accumulate in livers of subjects with NAFLD are not well characterized. Most of the published literature has focused on triglycerides accumulation as the key defect in NAFLD [6,7]. However, i
Comparative Evaluation of Whole Body and Hepatic Insulin Resistance Using Indices from Oral Glucose Tolerance Test in Morbidly Obese Subjects with Nonalcoholic Fatty Liver Disease  [PDF]
Kamran Qureshi,Ronald H. Clements,Fahad Saeed,Gary A. Abrams
Journal of Obesity , 2010, DOI: 10.1155/2010/741521
Abstract: Nonalcoholic Fatty Liver Disease (NAFLD) is the hepatic manifestation of metabolic syndrome and is a marker of Insulin Resistance (IR). Euglycemic-hyperinsulinemic clamp is the gold standard for measuring whole body IR (hepatic
Nonalcoholic fatty liver disease and obesity
Salgado Júnior, Wilson;Santos, José Sebasti?o dos;Sankarankutty, Ajith Kumar;Castro e Silva, Orlando de;
Acta Cirurgica Brasileira , 2006, DOI: 10.1590/S0102-86502006000700017
Abstract: purpose: the aim of this review is to update concepts of the nonalcoholic fatty liver disease (nafld) and to establish a relationship between this condition and obesity. methods: by means of a comprehensive literature review where special attention was devoted to articles published in the last 5 years, nafld is discussed in view of new concepts, diagnosis, staging, and treatment. results: nafld is emerging as one of the main causes of chronic liver disease and it is believed to be the hepatic component of the metabolic syndrome, whose central features include obesity, hyperinsulinemia, peripheral insulin resistance, diabetes, dyslipidemia, and hypertension. the surgical treatment of morbid obesity is one of the options available for the treatment of nafld. conclusion: nonalcoholic fatty liver disease is strongly related with obesity.
Etiopathogenesis of Nonalcoholic Steatohepatitis: Role of Obesity, Insulin Resistance and Mechanisms of Hepatotoxicity  [PDF]
Praveen Guturu,Andrea Duchini
International Journal of Hepatology , 2012, DOI: 10.1155/2012/212865
Abstract: Incidence of nonalcoholic fatty liver disease is increasing with an estimated prevalence of 20–30% in developed nations. This is leading to increased incidence of chronic liver disease, cirrhosis, and hepatocellular cancer. It is critical to understand the etiology and pathogenesis of any disease to create therapeutic targets and develop new treatments. In this paper we discuss the etiology and pathogenesis of nonalcoholic steatohepatitis with special focus on obesity, role of insulin resistance, and molecular mechanisms of hepatotoxicity.
Pathology of nonalcoholic fatty liver disease
D.G. Tiniakos, Ch. Kittas
Annals of Gastroenterology , 2007,
Abstract: Nonalcoholic fatty liver disease (NAFLD) may be the most common cause of chronic liver disease in Western countries, with an estimated prevalence of up to 24% in the general population. NAFLD is considered the hepatic manifestation of the metabolic syndrome and has been etiologically correlated with insulin resistance. The histopathological spectrum of NAFLD ranges from simple steatosis to nonalcoholic steatohepatitis (NASH), with or without fibrosis, and cirrhosis. Liver biopsy is the gold standard for diagnosing NASH in a patient with clinical features of NAFLD, image detected steatosis and chronically elevated liver enzymes. This review discusses the histopathological findings of NAFLD in adults and children, including features representing resolution of NASH following treatment and features of prognostic information. Additionally, current systems of semiquantitative assessment in NAFLD and NASH are reviewed and the concurrence of NAFLD and NASH with other chronic liver diseases, mainly hepatitis C, is discussed. Key words: steatosis, steatohepatitis, nonalcoholic, liver, pathology
Beneficial effects of treadmill training in experimental diabetic nerve regeneration
Malysz, Tais;Ilha, Jocemar;Nascimento, Patrícia Severo do;Angelis, Katia De;Schaan, Beatriz D'Agord;Achaval, Matilde;
Clinics , 2010, DOI: 10.1590/S1807-59322010001200017
Abstract: objectives: we investigated the effects of treadmill training (10 weeks) on hindlimb motor function and nerve morphometric parameters in diabetic rats submitted to sciatic nerve crush. materials and method: wistar rats (n = 64) were divided into the following groups: non-diabetic; trained non-diabetic; non-diabetic with sciatic nerve crush; trained non-diabetic with sciatic nerve crush; diabetic; trained diabetic; diabetic with sciatic nerve crush or trained diabetic with sciatic nerve crush. diabetes was induced by streptozotocin injection (50 mg/kg, iv). hindlimb motor function was evaluated weekly by assessing sciatic functional indices, and the proximal and distal portions of the sciatic nerve were used for morphometric analysis. results: at 13 weeks post-injury, the distal nerve portion of all injured groups and the proximal nerve portion of the diabetic with sciatic nerve crush group presented altered morphometric parameters such as decreased myelinated fiber diameter (~7.4 + 0.3μm vs ~4.8 + 0.2μm), axonal diameter (~5 + 0.2μm vs ~3.5 + 0.1μm) and myelin sheath thickness (~1.2 + 0.07μm vs ~0.65 + 0.07μm) and an increase in the percentage of area occupied by endoneurium (~28 + 3% vs ~60 + 3%). in addition, in the non-diabetic with sciatic nerve crush group the proximal nerve portion showed a decreased myelinated fiber diameter (7.4+0.3μm vs 5.8 + 0.3μm) and myelin sheath thickness (1.29 + 0.08μm vs 0.92 + 0.08μm). the non-diabetic with sciatic nerve crush, trained non-diabetic with sciatic nerve crush, diabetic with sciatic nerve crush and trained diabetic with sciatic nerve crush groups showed normal sciatic functional index from the 4th,4th,9th and 7th week post-injury, respectively. morphometric alterations in the proximal nerve portion of the diabetic with sciatic nerve crush and non-diabetic with sciatic nerve crush groups were either prevented or reverted to values similar to the non-diabetic group by treadmill training. conclusion: diabetic condition pro
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