Although low socioeconomic status (SES) and decreased muscle strength have been found to be associated with the risk factors of non-alcoholic fatty liver disease (NAFLD), including insulin resistance, obesity, and metabolic syndrome, the associations among SES, muscle strength, and NAFLD are still unclear. We aimed to investigate the combined effect of SES and relative handgrip strength (HGS) on the risk of NAFLD in middle-aged adults. Data from 5272 middle-aged adults who participated in the Korea National Health and Nutrition Examination Surveys (KNHANES) from 2014–2018 were analyzed. NAFLD was defined using the hepatic steatosis index (HSI) > 36 and the comprehensive NAFLD score (CNS) ≥ 40 in the absence of other causes of liver disease. SES was based on a self-reported questionnaire. Overall, individuals with low SES (odds ratio (OR) = 1.703, 95% confidence interval (CI): 1.424–2.037, p < 0.001) or low HGS (OR = 12.161, 95% CI: 9.548–15.488, p < 0.001) had a significantly higher risk of NAFLD. The joint association analysis showed that a low SES combined with a low HGS (OR = 2.479, 95% CI: 1.351–4.549, p = 0.003) further significantly increased the risk of NAFLD when adjusted for all the covariates, compared with individuals with a high SES and a high HGS (OR = 1). The current findings suggest that both low SES and low HGS were independently and synergistically associated with an increased risk of NAFLD in middle-aged Korean adults.

Doxorubicin is a highly effective chemotherapeutic agent widely used to treat a variety of cancers. However, the clinical application of doxorubicin is limited due to its adverse effects on several tissues. One of the most serious side effects of doxorubicin is cardiotoxicity, which results in life-threatening heart damage, leading to reduced cancer treatment success and survival rate. Doxorubicin-induced cardiotoxicity results from cellular toxicity, including increased oxidative stress, apoptosis, and activated proteolytic systems. Exercise training has emerged as a non-pharmacological intervention to prevent cardiotoxicity during and after chemotherapy. Exercise training stimulates numerous physiological adaptations in the heart that promote cardioprotective effects against doxorubicin-induced cardiotoxicity. Understanding the mechanisms responsible for exercise-induced cardioprotection is important to develop therapeutic approaches for cancer patients and survivors. In this report, we review the cardiotoxic effects of doxorubicin and discuss the current understanding of exercise-induced cardioprotection in hearts from doxorubicin-treated animals.

The quadriceps angle, knowns as the Q-angle, is an anatomical feature of the human body that is still largely unknown and unstudied despite its initial discovery in the 1950s. The strength disparities between male and female athletes are largely determined by the Q-angle. In spite of a growing number of women participating in sports such as track, tennis, soccer, gymnastics, basketball, volleyball, swimming, and softball, studies investigating injuries in this group are scanty. Even though the Q-angle has been the subject of many studies carried out all over the world, a review of the literature regarding its effects on health and injury risk in female athletes has not yet been completed. The aim of this review is to examine the crucial role of the Q-angle in the biomechanics of the knee joint and its effect on performance and injury risk, particularly in female athletes. Furthermore, we highlight the greater likelihood of knee-related injuries seen in female athletes being caused by the Q-angle. Athletes, coaches, healthcare professionals, and athletic trainers can better comprehend and prepare for the benefits and drawbacks resulting from the Q-angle by familiarizing themselves with the research presented in this review.

The mechanisms connecting obesity with type 2 diabetes, insulin resistance, nonalcoholic fatty liver disease, and cardiovascular diseases remain incompletely understood. The function of MAPK phosphatase-2 (MKP-2), a type 1 dual-specific phosphatase (DUSP) in whole-body metabolism, and how this contributes to the development of diet-induced obesity, type 2 diabetes (T2D), and insulin resistance is largely unknown. We investigated the physiological contribution of MKP-2 in whole-body metabolism and whether MKP-2 is altered in obesity and human fatty liver disease using MKP-2 knockout mice models and human liver tissue derived from fatty liver disease patients. We demonstrate that, for the first time, MKP-2 expression was upregulated in liver tissue in humans with obesity and fatty liver disease and in insulin-responsive tissues in mice with obesity. MKP-2-deficient mice have enhanced p38 MAPK, JNK, and ERK activities in insulin-responsive tissues compared with wild-type mice. MKP-2 deficiency in mice protects against diet-induced obesity and hepatic steatosis and was accompanied by improved glucose homeostasis and insulin sensitivity. Mkp-2^−/− mice are resistant to diet-induced obesity owing to reduced food intake and associated lower respiratory exchange ratio. This was associated with enhanced circulating insulin-like growth factor-1 (IGF-1) and stromal cell-derived factor 1 (SDF-1) levels in Mkp-2^−/− mice. PTEN, a negative regulator of Akt, was downregulated in livers of Mkp-2^−/− mice, resulting in enhanced Akt activity consistent with increased insulin sensitivity. These studies identify a novel role for MKP-2 in the regulation of systemic metabolism and pathophysiology of obesity-induced insulin resistance and fatty liver disease.

A small-molecule inhibitor of the phosphatase MKP5 identifies an allosteric site that enables specific targeting.

Obesity has reached global epidemic proportions and it affects the development of insulin resistance, type 2 diabetes, fatty liver disease and other metabolic diseases. Membrane lipids are important structural and signaling components of the cell membrane. Recent studies highlight their importance in lipid homeostasis and are implicated in the pathogenesis of fatty liver disease. Here, we discuss the numerous membrane lipid species and their metabolites including, phospholipids, sphingolipids and cholesterol, and how dysregulation of their composition and physiology contribute to the development of fatty liver disease. The development of new genetic and pharmacological mouse models has shed light on the role of lipid species on various mechanisms/pathways; these lipids impact many aspects of the pathophysiology of fatty liver disease and could potentially be targeted for the treatment of fatty liver disease.