Animal models have historically played a critical role in the exploration and characterization of disease pathophysiology and target identification and in the evaluation of novel therapeutic agents and treatments in vivo. Diabetes mellitus disease, commonly known as diabetes, is a group of metabolic disorders characterized by high blood glucose levels for a prolonged time. To avoid late complications of diabetes and related costs, primary prevention and early treatment are therefore necessary. Due to its chronic symptoms, new treatment strategies need to be developed, because of the limited effectiveness of the current therapies. We overviewed the pathophysiological features of diabetes in relation to its complications in type 1 and type 2 mice along with rat models, including Zucker Diabetic Fatty (ZDF) rats, BB rats, LEW 1AR1/-iddm rats, Goto-Kakizaki rats, chemically induced diabetic models, and Nonobese Diabetic mouse, and Akita mice model. The advantages and disadvantages that these models comprise were also addressed in this review. This paper briefly reviews the wide pathophysiological and molecular mechanisms associated with type 1 and type 2 diabetes, particularly focusing on the challenges associated with the evaluation and predictive validation of these models as ideal animal models for preclinical assessments and discovering new drugs and therapeutic agents for translational application in humans.

The objective of this research was to investigate skeletal muscle response to a chronic administration of stretch-shortening cycles (SSCs) in young and old rats. Dorsiflexor muscles of old (30 months, n = 5) and young (12 weeks, n = 6) rats were exposed 3 times/week for 4.5 weeks to a protocol of 80 maximal SSCs per exposure in vivo. Skeletal muscle response was characterized by isometric and dynamic performance, as well as by muscle wet mass and quantitative morphological analyses following the exposure period. The performance of the young and old groups was not statistically different at the start of the exposure. By the end of the exposure, however, a statistical difference was noted, as performance increased significantly in the young animals and decreased significantly in the old animals. Muscle wet mass of the left tibialis anterior (TA) in the treated limb was significantly greater in the youngthan in the old animals (p < 0.001), whereas there was no difference in the contra-lateral TA. No degenerative myofibers or changes in non-cellular interstitium were noted in either age group, but a significant increase was observed in the volume of the cellular interstitium in the exposed limb of the old animals (p = 0.01), which is indicative of an inflammatory response. Thus, a chronic exposure of SSCs results in significant performance increase and muscle hypertrophy in young animals, and a significant performance decrease and an increased cellular interstitial response in old animals. These findings suggest that age may impair the ability of skeletal muscle to adapt to repetitive mechanical loading, even in the absence of degeneration.

We conducted a systematic literature review and meta-analysis to assess the chronic effects of the sequence of concurrent strength and endurance training on selected important physiological and performance parameters, namely lower body 1 repetition maximum (1RM) and maximal aerobic capacity (VOmax/peak). Based on predetermined eligibility criteria, chronic effect trials, comparing strength-endurance (SE) with endurance-strength (ES) training sequence in the same session were included. Data on effect sizes, sample size and SD as well other related study characteristics were extracted. The effect sizes were pooled using, Fixed or Random effect models as per level of heterogeneity between studies and a further sensitivity analyses was carried out using Inverse Variance Heterogeneity (IVHet) models to adjust for potential bias due to heterogeneity. Lower body 1RM was significantly higher when strength training preceded endurance with a pooled mean change of 3.96 kg (95%CI: 0.81 to 7.10 kg). However, the training sequence had no impact on aerobic capacity with a pooled mean difference of 0.39 ml.kg.min (95%CI: -1.03 to 1.81 ml.kg.min). Sequencing strength training prior to endurance in concurrent training appears to be beneficial for lower body strength adaptations, while the improvement of aerobic capacity is not affected by training order.

Aging is a complex process characterized by progressive multisystem derangement predisposing individuals to increased risk of developing negative health outcomes. Sarcopenia is the age-related decline of muscle mass and function/strength and represents a highly prevalent correlate of aging. Several factors have been indicated to play a role in the onset and progression of sarcopenia; however, its pathophysiology is still unclear. Physical exercise is to date one of the few strategies able to improve muscle health in old age through multiple metabolic and transcriptional adaptations. Although the benefits of different exercise modalities on the function and structure of aged myocytes is acknowledged, the cellular and molecular mechanisms underlying such effects are not yet fully identified. Here, we briefly overview the current knowledge on the biochemical pathways associated with the onset and progression of sarcopenia. We subsequently describe the effects of exercise on relevant signaling pathways involved in sarcopenia pathophysiology.