BackgroundAlthough hypercaloric interventions are associated with nutritional, endocrine, metabolic, and cardiovascular disorders in obesity experiments, a rational distinction between the effects of excess adiposity and the individual roles of dietary macronutrients in relation to these disturbances has not previously been studied. This investigation analyzed the correlation between ingested macronutrients (including sucrose and saturated and unsaturated fatty acids) plus body adiposity and metabolic, hormonal, and cardiovascular effects in rats with diet-induced obesity.MethodsNormotensive Wistar-Kyoto rats were submitted to Control (CD; 3.2 Kcal/g) and Hypercaloric (HD; 4.6 Kcal/g) diets for 20 weeks followed by nutritional evaluation involving body weight and adiposity measurement. Metabolic and hormonal parameters included glycemia, insulin, insulin resistance, and leptin. Cardiovascular analysis included systolic blood pressure profile, echocardiography, morphometric study of myocardial morphology, and myosin heavy chain (MHC) protein expression. Canonical correlation analysis was used to evaluate the relationships between dietary macronutrients plus adiposity and metabolic, hormonal, and cardiovascular parameters.ResultsAlthough final group body weights did not differ, HD presented higher adiposity than CD. Diet induced hyperglycemia while insulin and leptin levels remained unchanged. In a cardiovascular context, systolic blood pressure increased with time only in HD. Additionally, in vivo echocardiography revealed cardiac hypertrophy and improved systolic performance in HD compared to CD; and while cardiomyocyte size was unchanged by diet, nuclear volume and collagen interstitial fraction both increased in HD. Also HD exhibited higher relative β-MHC content and β/α-MHC ratio than their Control counterparts. Importantly, body adiposity was weakly associated with cardiovascular effects, as saturated fatty acid intake was directly associated with most cardiac remodeling measurements while unsaturated lipid consumption was inversely correlated with these effects.ConclusionHypercaloric diet was associated with glycemic metabolism and systolic blood pressure disorders and cardiac remodeling. These effects directly and inversely correlated with saturated and unsaturated lipid consumption, respectively.
Tetanus is characterized by high case fatality rates in horses. Comprehensive case series studies involving equine tetanus from different geographic areas enable the evaluation of prognosis, efficacy of treatment, and control measures. We retrospectively investigated some selected epidemiological data (breed, age, gender, use of the horses, history of vaccination, seasonality, presence of wound/history of surgical procedures, clinical outcomes) and main clinical aspects (clinical signs, incubation period, length of hospitalization, and period between onset signs and hospitalization) in 70 cases of equine tetanus over 1990-2015, with emphasis in the association between these data and the clinical outcomes. High mortality rate (72.9%) was observed in this study. Forty (57.1%) horses presented history of wounds or surgical procedures related with tetanus, represented mainly by lesions in the hind limbs (42.5%), front limbs (15.0%), umbilical infections (7.1%), castration (4.3%), and face wounds (4.3%). Hyperesthesia, limb spasticity, cervical stiffness, tetanic spasms, and restriction of jaw movement were the main consistent clinical signs. Besides no statistical association, all the horses with umbilical infections, wounds in face, prolonged recumbency, sweating, dysphagia/aphagia died, and together with delay between onset of first clinical signs and prompt veterinary assistance (< 5 days) were considered indicative of poor prognosis; whereas there was a significant association (p=0.001) between survival and length of hospitalization > 7 days, seemed as an evidence of good prognosis. The high mortality rate of tetanus, even in horses under specific treatment, highlight the need for early diagnosis, prompt veterinary assistance, and establishment of prophylatic measures in equine farms.
Vocal symptoms, reported by 27.8% of the patients on the 1st post decreased to 7% in 6 months. In the acoustic analysis, f0 and APQ were decreased. Transient paralysis of the vocal folds secondary to recurrent and superior laryngeal nerve injury occurred in, respectively, 21% and 1.3% of the patients, decreasing to 6.6% and 0% after 6 months.
Heart failure (HF) is characterized by limited exercise tolerance, skeletal muscle atrophy, a shift toward fast muscle fiber, and myogenic regulatory factor (MRF) changes. Reactive oxygen species (ROS) also contribute to target organ damage in this syndrome. In this study, we investigated and compared morphofunctional characteristics and gene expression in Soleus (SOL--oxidative and slow twitching muscle) and in Extensor Digitorum Longus (EDL--glycolytic and fast twitching muscle) during HF. Two groups of rats were used: control (CT) and heart failure (HF), induced by a single injection of monocrotaline. MyoD and myogenin gene expression were determined by RT-qPCR, and MHC isoforms by SDS-PAGE; muscle fiber type frequency and cross sectional area (CSA) were analyzed by mATPase. A biochemical study was performed to determine lipid hydroperoxide (LH), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD); myography was used to determine amplitude, rise time, fall time, and fatigue resistance in both muscles. HF showed SOL and EDL muscle atrophy in all muscle fiber types; fiber frequency decreased in type IIC and muscle contraction fall time increased only in SOL muscle. Myogenin mRNA expression was lower in SOL and myoD decreased in HF EDL muscle. LH increased, and SOD and GSH-Px activity decreased only in HF SOL muscle. HF EDL muscle did not present changes in MHC distribution, contractile properties, HL concentration, and antioxidant enzyme activity. In conclusion, our results indicate that monocrotaline induced HF promoted more prominent biochemical, morphological and functional changes in SOL (oxidative and slow twitching muscle). Although further experiments are required to better determine the mechanisms involved in HF pathophysiology, our results contribute to understanding the muscle-specific changes that occur in this syndrome.
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