Abstract
Osteoarthritis (OA) and type 2 diabetes mellitus (T2D) are two of the most widespread chronic diseases. OA and T2D have common epidemiologic traits, are considered heterogenic multifactorial pathologies that develop through the interaction of genetic and environmental factors, and have common risk factors. In addition, both of these diseases often manifest in a single patient. Despite differences in clinical manifestations, both diseases are characterized by disturbances in cellular metabolism and by an insulin-resistant state primarily associated with the production and utilization of energy. However, currently, the primary cause of OA development and progression is not clear. In addition, although OA is manifested as a joint disease, evidence has accumulated that it affects the whole body. As pathological insulin resistance is viewed as a driving force of T2D development, now, we present evidence that the molecular and cellular metabolic disturbances associated with OA are linked to an insulin-resistant state similar to T2D. Moreover, the alterations in cellular energy requirements associated with insulin resistance could affect many metabolic changes in the body that eventually result in pathology and could serve as a unified mechanism that also functions in many metabolic diseases. However, these issues have not been comprehensively described. Therefore, here, we discuss the basic molecular mechanisms underlying the pathological processes associated with the development of insulin resistance; the major inducers, regulators, and metabolic consequences of insulin resistance; and instruments for controlling insulin resistance as a new approach to therapy.
Highlights
Osteoarthritis (OA) and diabetes mellitus (DM) represent the most prevalent chronic disorders
Erefore, Type 2 diabetes mellitus (T2D) and OA are both associated with patient age, low-grade inflammation, and obesity and result in disturbances in cellular metabolism; these disorders might have common pathophysiological mechanisms [1]. ese similarities suggest that common approaches could be applied to ameliorate the metabolic imbalance associated with these diseases. erefore, the aim of the study was to demonstrate that OA is not a disease solely of a single joint but like T2D is a pathology of the whole body, which results from insulin resistance-related traits that develop before the onset of the disease
Receptor activation leads to the phosphorylation of tyrosine residues on adaptor proteins, members of the insulin receptor substrate family (IRS), which promote signalling to downstream targets [19]
Summary
Osteoarthritis (OA) and diabetes mellitus (DM) represent the most prevalent chronic disorders. OA is presently viewed as a chronic, systemic disease with slow progression and involves whole joint destruction that mainly includes degradation of hyaline articular cartilage, ligaments, menisci in the knee, hypertrophic changes of the joint capsule as well as subchondral bone remodelling, osteophyte formation, and synovial inflammation. It is accompanied by pain, dysfunction of the lower extremities, and joint deformities [2]. Type 1 diabetes mellitus (T1D) is a chronic immune-mediated disease characterized by the selective loss of insulin-producing-β-cells in the pancreatic islets in genetically susceptible individuals resulting in severe insulin deficiency. T2D development involves a progressive disturbance in glucose tolerance, which is associated with initial hyperplasia of the pancreatic islets followed by the proliferation of Langerhans β-cells. ese processes are accompanied by an inflammatory response that induces the accumulation of the extracellular matrix (fibrosis) and the apoptotic death of islet β-cells, resulting in the progressive failure of β-cells to produce sufficient levels of insulin, followed by a decrease in insulin-stimulated glucose uptake and long-lasting hyperglycaemia. e concomitant development of osmotic and oxidative stresses produces lesions in the kidney, nervous system, and other tissues, which negatively affect the patient’s lifespan [4]
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