Adipose

links: reference: https://men-elite.com/2018/06/15/uncoupling-secret-to-fat-loss-and-health/ 5-14-2021

Body Fat #

Adipose tissue fatty acids have a half-life of around 2-4 years.

• This seems ironic at first, but increasing Fatty Acid Oxidation won’t help you lose body fat. You’ll just burn less carbs. RPF.
• Improving Glucuronidation is probably a good attack surface for losing body fat. FAO inhibitors do usually improve liver function though, maybe due to ROS or endorphins or whatever.
• Role of AMP-activated protein kinase in adipose tissue metabolism and inflammation
  • Suggests obese adipose tissue is necrotic and M1 phenotype with lower levels of Adiponectin.
• Proteomics analysis of adipose depots after intermittent fasting reveals visceral fat preservation mechanisms
  • Enrichment analysis highlights downregulation of inflammatory collagen IV specifically in vWAT, allowing improved insulin sensitivity.
    • This is probably how EODF downregulates Lipolysis in visceral white adipose.
      • Reminds me of exactly what tyw’s claims are: https://raypeatforum.com/community/threads/tyw-said-something-that-makes-alot-of-sense.15816/post-215576
        • Cortisol is high, FFA is high, insulin is at rock-bottom levels …. similarly, put someone on a diet that is 80% calories by fat (the classic ketogenic diet), feed them to eucaloric sufficiency, and systemic insulin release is going to be very low.
        • Or how about take an obese person, put them on a ketogenic diet, induce physiologic Insulin Resistance, which thereby prevents net ingress of calories into fatty tissue, thereby causing easy loss of that fatty tissue
          • https://bodyrecomposition.com/fat-loss/insulin-resistance-fat-loss
        • Feed a low-PUFA, SFA-dominated, ketogenic diet to a diabetic, watch them lose fat, stay systemic insulin resistant (a good thing in the context of low glucose availability, because it spares glucose for the tissues that need it, and thus prevent the stress response), and then eventually become non-diabetic, and can transition to a different diet.
          • HOW?
        • I agree with this assessment, so long as caloric excess is the case: https://high-fat-nutrition.blogspot.com/2017/02/musing-about-linoleic-acid.html
          • Linoleic Acid produces excessive whole-body insulin sensitivity. But then, adipocytes distend (enlarge) and release FFAs, causing insulin resistance.
            • Whole-body is spooky. It would be elegant to assume this is restricted to fatty tissue.
          • I think this is their only claim as to how it improves glucose tolerance.
  • Increase in mitochondrial protein content in sWAT and vWAT, correlated with increased fatty acid synthesis enzymes in WAT but not brown adipose.
• Intermittent Fasting Induces Hypothalamic Modifications Resulting in Low Feeding Efficiency, Low Body Mass and Overeating
  • Increased expression of AgRP/NPY in the hypothalamus.
• Selective mobilization of adipose tissue fatty acids during energy depletion in the rat
  • Fasting resulted in depletion of unsaturated fats like AA, ALA, DHA, and a storing of VLCFA.
  • The more double bonds with the shorter chain length, the higher the polarity of the Fatty Acid, thus the easier it is for Hormone-sensitive lipase to liberate the fat from the tissues