New Insights and Potential Therapeutic Interventions in Metabolic Diseases

Clemente-Suárez, Vicente Javier; Martín-Rodríguez, Alexandra; Redondo-Flórez, Laura; López-Mora, Clara; Yáñez-Sepúlveda, Rodrigo; Tornero-Aguilera, José Francisco

doi:10.3390/ijms241310672

Cited by 32 publications

(8 citation statements)

References 356 publications

(405 reference statements)

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“…A multifaceted strategy is required for preventing or controlling metabolic disorders because of the complex interplay of environmental, genetic, and epigenetic factors in the development of metabolic diseases [ 33 ]. We investigated the differential expression of serum proteome profiles and possible mechanisms in the non-obese and obese groups ( Figure 4 and Figure 5 and Table 4 ).…”

Section: Discussionmentioning

confidence: 99%

Role of Dietary Factors on DNA Methylation Levels of TNF-Alpha Gene and Proteome Profiles in Obese Men

Boonrong,

Roytrakul,

Shantavasinkul

et al. 2024

Nutrients

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Integrated omics-based platforms from epigenomics and proteomics technologies are used to identify several important mechanisms in obesity etiology, food components, dietary intake, regulation of biological pathways, and potential new intervention targets. Therefore, this study aimed to analyze whether dietary factors involved in the methylation of tumor necrosis factor (TNF)-α are implicated in differential protein expression in people with normal weight and obesity. Methods: The participants were classified into the non-obese (N = 100) and obese (N = 133) groups. DNA methylation levels of the TNF-alpha gene and proteomics were analyzed using the pyrosequencing method and LC-MS-MS, respectively. Results: Comparison between geometric means of DNA methylation of TNF-α showed lower levels in subjects with obesity than in those without obesity (p < 0.05). There were associations between dietary factors and some metabolic syndrome components and TNF-α DNA methylation levels. Proteomic analysis showed important signaling pathways related to obesity, with 95 significantly downregulated proteins and 181 upregulated proteins in the non-obese group compared with the obese group. Conclusion: This study shows an association between the dietary factors involved in the methylation of TNF-α and differential protein expression related to obesity. However, a large sample size in future studies is required to confirm our results.

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Section: Discussionmentioning

confidence: 99%

Role of Dietary Factors on DNA Methylation Levels of TNF-Alpha Gene and Proteome Profiles in Obese Men

Boonrong,

Roytrakul,

Shantavasinkul

et al. 2024

Nutrients

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“…Cognitive behavioral therapy, motivational interviewing, and mindfulness-based strategies can also assist people with metabolic illnesses and FD to achieve long-term lifestyle adjustments. These therapies aim to address psychological obstacles, increase self-efficacy, reduce stress, and facilitate behavior transformation to enhance long-term adherence to good behaviors, which can contribute to FD and MetS treatment [115].…”

Section: Future Perspectivesmentioning

confidence: 99%

The Association between Functional Dyspepsia and Metabolic Syndrome—The State of the Art

Volarić,

Šojat,

Majnarić

et al. 2024

IJERPH

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Functional dyspepsia is a common functional disorder of the gastrointestinal tract that is responsible for many primary care visits. No organic changes have been found to explain its symptoms. We hypothesize that modern lifestyles and environmental factors, especially psychological stress, play a crucial role in the high prevalence of functional dyspepsia and metabolic syndrome. While gastrointestinal tract diseases are rarely linked to metabolic disorders, chronic stress, obesity-related metabolic syndrome, chronic inflammation, intestinal dysbiosis, and functional dyspepsia have significant pathophysiological associations. Functional dyspepsia, often associated with anxiety and chronic psychological stress, can activate the neuroendocrine stress axis and immune system, leading to unhealthy habits that contribute to obesity. Additionally, intestinal dysbiosis, which is commonly present in functional dyspepsia, can exacerbate systemic inflammation and obesity, further promoting metabolic syndrome-related disorders. It is worth noting that the reverse is also true: obesity-related metabolic syndrome can worsen functional dyspepsia and its associated symptoms by triggering systemic inflammation and intestinal dysbiosis, as well as negative emotions (depression) through the brain–gut axis. To understand the pathophysiology and deliver an effective treatment strategy for these two difficult-to-cure disorders, which are challenging for both caregivers and patients, a psychosocial paradigm is essential.

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“…The significance of multidisciplinary interventions in modulating the psychophysiological response of patients cannot be overstated [ 288 , 289 , 290 ]. By bringing together professionals from various disciplines, such as psychiatrists, psychologists, neurologists, and therapists, a comprehensive and holistic approach can be adopted to address the complex interplay between mental and physical health [ 291 , 292 , 293 , 294 , 295 ]. This collaborative effort allows for a more nuanced understanding of the phylogenetic and behavioral bases of the disease, encompassing both genetic predispositions and environmental factors that contribute to its development [ 296 , 297 ].…”

Section: Therapeutic Strategies For Modulating Neuro-vulnerabilitymentioning

confidence: 99%

Neuro-Vulnerability in Energy Metabolism Regulation: A Comprehensive Narrative Review

et al. 2023

Self Cite

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This comprehensive narrative review explores the concept of neuro-vulnerability in energy metabolism regulation and its implications for metabolic disorders. The review highlights the complex interactions among the neural, hormonal, and metabolic pathways involved in the regulation of energy metabolism. The key topics discussed include the role of organs, hormones, and neural circuits in maintaining metabolic balance. The review investigates the association between neuro-vulnerability and metabolic disorders, such as obesity, insulin resistance, and eating disorders, considering genetic, epigenetic, and environmental factors that influence neuro-vulnerability and subsequent metabolic dysregulation. Neuroendocrine interactions and the neural regulation of food intake and energy expenditure are examined, with a focus on the impact of neuro-vulnerability on appetite dysregulation and altered energy expenditure. The role of neuroinflammation in metabolic health and neuro-vulnerability is discussed, emphasizing the bidirectional relationship between metabolic dysregulation and neuroinflammatory processes. This review also evaluates the use of neuroimaging techniques in studying neuro-vulnerability and their potential applications in clinical settings. Furthermore, the association between neuro-vulnerability and eating disorders, as well as its contribution to obesity, is examined. Potential therapeutic interventions targeting neuro-vulnerability, including pharmacological treatments and lifestyle modifications, are reviewed. In conclusion, understanding the concept of neuro-vulnerability in energy metabolism regulation is crucial for addressing metabolic disorders. This review provides valuable insights into the underlying neurobiological mechanisms and their implications for metabolic health. Targeting neuro-vulnerability holds promise for developing innovative strategies in the prevention and treatment of metabolic disorders, ultimately improving metabolic health outcomes.

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New Insights and Potential Therapeutic Interventions in Metabolic Diseases

Cited by 32 publications

References 356 publications

Role of Dietary Factors on DNA Methylation Levels of TNF-Alpha Gene and Proteome Profiles in Obese Men

Role of Dietary Factors on DNA Methylation Levels of TNF-Alpha Gene and Proteome Profiles in Obese Men

The Association between Functional Dyspepsia and Metabolic Syndrome—The State of the Art

Neuro-Vulnerability in Energy Metabolism Regulation: A Comprehensive Narrative Review

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