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<article xlink="http://www.w3.org/1999/xlink" dtd-version="1.0" article-type="family-medicine" lang="en">
<front>
<journal-meta>
<journal-id journal-id-type="publisher">JOHS</journal-id>
<journal-id journal-id-type="nlm-ta">Journ of Health Scien</journal-id>
<journal-title-group>
<journal-title>Journal of HealthCare Sciences</journal-title>
<abbrev-journal-title abbrev-type="pubmed">Journ of Health Scien</abbrev-journal-title>
</journal-title-group>
<issn pub-type="ppub">2231-2196</issn>
<issn pub-type="opub">0975-5241</issn>
<publisher>
<publisher-name>Radiance Research Academy</publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id pub-id-type="publisher-id">299</article-id>
<article-id pub-id-type="doi">http://dx.doi.org/10.52533/JOHS.2024.41002</article-id>
<article-id pub-id-type="doi-url"/>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Family Medicine</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>Obesity-Induced Inflammation and Its Role in the Development of Insulin Resistance
</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Abdullah</surname>
<given-names>Marwah Yakoop</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>AlQwaidi</surname>
<given-names>Saad Daham</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Alshehri</surname>
<given-names>Aisha Mohammed</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Alamry</surname>
<given-names>Fatimah Ali</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Alamri</surname>
<given-names>Raghad Saad</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Alsolbi</surname>
<given-names>Zainab Khaleel</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Alqurashi</surname>
<given-names>Bushra Haidar</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Aldandan</surname>
<given-names>Yousef Ali</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Alrashidi</surname>
<given-names>Awadh Muhaysin</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Aljumaie</surname>
<given-names>Maha Ayed</given-names>
</name>
</contrib>
</contrib-group>
<pub-date pub-type="ppub">
<day>6</day>
<month>10</month>
<year>2024</year>
</pub-date>
<volume>4</volume>
<issue>10</issue>
<fpage>448</fpage>
<lpage>454</lpage>
<permissions>
<copyright-statement>This article is copyright of Popeye Publishing, 2009</copyright-statement>
<copyright-year>2009</copyright-year>
<license license-type="open-access" href="http://creativecommons.org/licenses/by/4.0/">
<license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution (CC BY 4.0) Licence. You may share and adapt the material, but must give appropriate credit to the source, provide a link to the licence, and indicate if changes were made.</license-p>
</license>
</permissions>
<abstract>
<p>Obesity is a leading global health issue closely associated with metabolic disorders, including insulin resistance and Type 2 Diabetes Mellitus (T2DM). A central mechanism linking obesity to these metabolic dysfunctions is chronic, low-grade inflammation. In individuals with obesity, adipose tissue becomes dysfunctional, characterized by adipocyte hypertrophy, hypoxia, and the infiltration of immune cells such as macrophages. These changes lead to the release of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-__ampersandsignalpha;), interleukin-6 (IL-6), and monocyte chemoattractant protein-1 (MCP-1), which interfere with insulin signaling pathways. The activation of inflammatory pathways like nuclear factor-kappa B (NF-__ampersandsignkappa;B) and c-Jun N-terminal kinase (JNK) promotes the serine phosphorylation of insulin receptor substrates (IRS), impairing their ability to propagate insulin signals effectively. This disruption leads to reduced glucose uptake in tissues such as the liver, muscle, and adipose tissue, contributing to systemic insulin resistance. Additionally, the NLRP3 inflammasome pathway exacerbates inflammation by activating caspase-1 and increasing IL-1__ampersandsignbeta; production, further impairing insulin signaling. Free fatty acids (FFAs) released from hypertrophic adipocytes also play a significant role in perpetuating inflammation and disrupting insulin sensitivity. FFAs activate toll-like receptor 4 (TLR4) on immune cells, enhancing the inflammatory response and contributing to ectopic fat deposition in non-adipose tissues, further promoting insulin resistance. Understanding the mechanisms linking obesity-induced inflammation to insulin resistance provides insight into potential therapeutic interventions. Targeting chronic inflammation, modulating cytokine production, and addressing adipose tissue dysfunction may improve insulin sensitivity and help manage obesity-related metabolic disorders. This highlights the need for a multifaceted approach to treat obesity and its associated complications, particularly focusing on reducing inflammation to mitigate the risk of insulin resistance and T2DM.
</p>
</abstract>
<kwd-group>
<kwd>obesity</kwd>
<kwd> inflammation</kwd>
<kwd> insulin resistance</kwd>
<kwd> adipose tissue dysfunction</kwd>
<kwd> pro-inflammatory cytokines</kwd>
</kwd-group>
</article-meta>
</front>
</article>