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Insulin Resistance and Its Biochemical Basis in Metabolic Syndrome

  • Dhruvi Hasnani,
  • Sarai Iglesias Fortes,
  • Angela Cristina Lockwood López,
  • Vipul Chavda

摘要

The chapter delves into biochemical underpinnings of insulin resistance within the metabolic syndrome framework, a growing health concern marked by obesity, hyperglycemiaHyperglycemia, hyperlipidemia, and hypertension, leading to cardiovascular disease risks. Insulin resistance is explored through complex interplay of genetic predispositions, environmental factors, and lifestyle choices affecting glucose and lipid metabolismLipid metabolism. Highlighting the disruption of insulin signaling pathwaysSignaling pathways, particularly the MAPK and PI3K/AktPI3K/AKT routes, chapter outlines how these alterations contribute to diminished glucose uptake and systemic metabolic disturbances. The document also underscores the molecular mechanisms and therapeutic targets for insulin resistance, focusing on the IRS → Akt → Foxo1 signaling cascadeIRS→Akt→Foxo1 signaling cascade as a potential intervention point to mitigate metabolic disturbances. Clinical implications of insulin resistance span across a spectrum of conditions including type 2 diabetesDiabetes (T2DM), cardiovascular diseases, Non-Alcoholic Fatty LiverLiver diseasesnon-alcoholic fatty liver disease Disease/Non-Alcoholic SteatohepatitisSteatohepatitis (NAFLD/NASH), obesity, PCOSPCOS, dyslipidemiaDyslipidemia, and even certain cancers, establishing insulin resistance not just as a metabolic defect but as a central contributor to widespread health issues. Through a detailed exploration of signaling pathwaysSignaling pathways and the mechanisms leading to insulin resistance, the chapter provides insight into the molecular basis of the condition, offering a foundation for future therapeutic strategies aimed at combating metabolic syndrome and its far-reaching implications on public health.