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Metabolic Syndrome - Coggle Diagram

- - - - NPY (brain)
      - AGRP (brain)
      - Ghrelin (periphery)
    - - Alpha-MSH (brain)
      - Leptin (periphery)
- - - - Nephropathy
      - Retinopathy
      - Neuropathy
      - Poor wound healing / increased risk of infection
    - - Increased cell proliferation
      - decreased apoptosis
  - - - Early detection and preventing progression
    - - Improve life quality and reduce symptoms
    - - Prevent onset
- - - - Glucose uptake via GLUT4 (fast because proteins needed already synthesised)
      - Glycogen synthesis via glycogen synthase (fast as proteins needed already synthesised)
      - Causes fatty acid synthesis (slow because requires gene expression to produce enzymes)
  - - - Transition if no intervention, characterised by the death of any REMAINING beta cells
      - A gradual but not universal process (depends on genetics and lifestyle habits too)
        
        Primary feature is insulin resistance (when beta cells begin to die, so insufficient insulin is produced) due to lack of signal transduction despite presence of insulin (aberrant phosphorylation of IRS-1)
        
        Beta cell death may also be accompanied by beta cell dysfunction (i.e. faulty insulin exocytosis, esp. due to obesity)
        
        Dominant negative mutation in TCF7L2 gene may lead to decreased physiological beta cell mass (increased risk of T2D)
    - - Fasting blood sugar test
      - Glycated haemoglobin test
      - Oral glucose tolerance test
  - - - Important – as BMI increases, risk of T2D increases
- - - - indicates visceral fat
      - obesity as risk factor for MetSy
    - - high Apo B
      - more VLDL (risk factor)
      - LDL more atherosclerotic
    - - higher risk of CV diseases
- - - - unique capacity to digest plant polysaccharide (with PUL)
  - - - e.g. decreased SCFA
- - - - Exercise, Alcohol, Smoking, Diet
    - - Treatment specific for T2D & the heart diseases
    - - New range of rational targets – inhibitors of Ser/Thr kinases
      - Replication of existing β cells
      - Use of stem-cell derived β cells
      - Reprogramming cells
      - miRNA regulation to modulate insulin signaling