Emerging evidence strongly suggests that gut microbiota dysbiosis plays a significant role in the development and progression of both type 1 and type 2 diabetes mellitus. Quantitative and qualitative changes in the intestinal microbiota’s composition are linked to these distinct pathomechanisms. In type 1 diabetes mellitus, dysbiosis is thought to initiate or accelerate the autoimmune destruction of pancreatic beta cells. This may occur through increased intestinal permeability, which allows microbial components and endotoxins to enter the systemic circulation. This exposure triggers inflammatory and autoimmune responses in individuals who are genetically predisposed. Conversely, in type 2 diabetes mellitus, gut dysbiosis contributes significantly to the characteristic metabolic derangements. Specific microbial shifts can lead to impaired energy metabolism, contributing to insulin resistance in peripheral tissues. Furthermore, dysbiosis is associated with the altered production of microbial metabolites, such as short-chain fatty acids, and the induction of low-grade chronic inflammation, which contribute to the pathogenesis of type 2 diabetes mellitus. Hyperglycemia, dyslipidemia and other metabolic changes also influence the gut microbiota. Understanding these type-specific microbial roles offers potential for novel diagnostic and therapeutic strategies.

Background: The diagnostic value of surface electromyography (sEMG) for identifying muscles affected by myofascial trigger points (TrPs) remains controversial. However, advances in pain neurophysiology and discussions regarding TrPs within the International Classification of Diseases (ICD-11) have renewed interest in objective diagnostic approaches. Objective: To synthesize current evidence on the diagnostic utility of sEMG for detecting TrP-related muscle alterations across different electromyographic signal analysis domains. Methods: A scoping review was conducted following JBI guidance and PRISMA-ScR guidelines. PubMed, Scopus, Web of Science, CINAHL and Cochrane were searched for studies involving adults with symptomatic or asymptomatic TrPs, myofascial pain syndrome, or TrP-related referred pain. Fifteen studies met the inclusion criteria. Analyses included amplitude-, frequency-, time–frequency-, and spatial-domain sEMG parameters. Results: Muscles affected by TrPs showed increased resting electromyographic activity and reduced activation during maximal voluntary contraction in several studies. Frequency domain analyses indicated changes in median frequency and muscle fatigue index, whereas time–frequency analyses suggested redistribution of sEMG signal energy toward lower-frequency components or altered spectral power during experimentally provoked referred pain. Spatial analyses revealed altered activation patterns, although these findings did not consistently correspond with TrP anatomical locations. Overall, the limited number of studies assessing diagnostic sensitivity and specificity prevents firm conclusions. Conclusions: sEMG may be useful as a non-invasive complementary tool for functional assessment and monitoring of TrP-related muscle dysfunction. However, current evidence does not support its use as a standalone diagnostic method. Time–frequency, machine learning-supported and spatial analyses appear promising for future clinical research, but standardized protocols and external validation are required before clinical diagnostic criteria can be proposed.

Introduction: The increasing prevalence of diabetes mellitus (DM) has intensified research into its mechanisms and complications. Alterations in gut microbiota are considered an environmental factor influencing the onset, progression, and complications of diabetes. This review summarizes current evidence on the role of microbiota in diabetes and its outcomes. Methods: This literature review was conducted using English-language articles from PubMed and Google Scholar, focusing on original research and reviews, primarily published within the last 10 years. Key search terms included “type 1 diabetes mellitus,” “type 2 diabetes mellitus,” “gut microbiota dysbiosis,” and related metabolic and complication terms. Both animal and human studies were included. Results: Current studies reveal a strong correlation between gut microbiota alterations and diabetes and its complications. Dysbiosis, characterized by reduced bacterial diversity, is observed in both type 1 (T1DM) and type 2 diabetes (T2DM) patients. In T1DM, dysbiosis may contribute to immune dysregulation and increased intestinal permeability. In T2DM, lower bacterial diversity is linked to insulin resistance and obesity. Dysbiosis is also directly associated with diabetic retinopathy and contributes to nephropathy, neuropathy, and ischemic heart disease. Discussion: These findings suggest that gut microbiota alterations may play a role in diabetes pathogenesis and its complications, indicating potential targets for therapeutic modulation. However, causal relationships remain to be fully clarified. Conclusion: Although progress has been made, the precise role of gut bacteria in diabetes remains unclear. A better understanding of these mechanisms is crucial for developing diagnostic and therapeutic strategies, and further human studies are needed to confirm findings from animal models.