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<blockquote data-quote="KenMacK" data-source="post: 2052650" data-attributes="member: 506757"><p>Also, I might add or clarify, the condition of lipotoxicity (which I consider an effect rather than cause of degenerated organ function -- especially adipose de novo lipogenesis -- in MetS) is known to include a downregulation of glucose transport (via GLUT4) in insulin-sensitive tissues -- hence, these tissues, including fatty liver, are technically insulin-resistant to some quantifiable extent -- the primary consequent metabolic degeneration is of FA (fatty-acid) metabolism. This can drop to < 20% of normal. On the other hand, in the same tissues, glucose metabolism remains close to normal at >> 80%. In tissues evolved to rely upon FAs, such as muscle, there is a switch to reliance upon glucose for ATP production and this robs huge amounts of BG from the brain. Hence, constant brain fuel crises and carb craving to rapidly resupply the blood with glucose. </p><p>With this minor qualification, I would challenge anyone to provide evidence to refute my claim that the diabetic liver is not significantly or meaningfully insulin resistant. </p><p>On the other hand, it is catastrophic for the entire body to have a fatty liver, which means that the liver cannot engage properly in the normal FA metabolism of the fasted or semi-fasted states, including ketosis. Hence, the brain is not supplied with the appropriate alternative fuel of ketones and the liver cannot rapidly respond to the overdemand for blood glucose induced by lipotoxicity in major, high-mass high-energy tissues such as muscle without direct resupply of glucose portally (from meals).</p></blockquote><p></p>
[QUOTE="KenMacK, post: 2052650, member: 506757"] Also, I might add or clarify, the condition of lipotoxicity (which I consider an effect rather than cause of degenerated organ function -- especially adipose de novo lipogenesis -- in MetS) is known to include a downregulation of glucose transport (via GLUT4) in insulin-sensitive tissues -- hence, these tissues, including fatty liver, are technically insulin-resistant to some quantifiable extent -- the primary consequent metabolic degeneration is of FA (fatty-acid) metabolism. This can drop to < 20% of normal. On the other hand, in the same tissues, glucose metabolism remains close to normal at >> 80%. In tissues evolved to rely upon FAs, such as muscle, there is a switch to reliance upon glucose for ATP production and this robs huge amounts of BG from the brain. Hence, constant brain fuel crises and carb craving to rapidly resupply the blood with glucose. With this minor qualification, I would challenge anyone to provide evidence to refute my claim that the diabetic liver is not significantly or meaningfully insulin resistant. On the other hand, it is catastrophic for the entire body to have a fatty liver, which means that the liver cannot engage properly in the normal FA metabolism of the fasted or semi-fasted states, including ketosis. Hence, the brain is not supplied with the appropriate alternative fuel of ketones and the liver cannot rapidly respond to the overdemand for blood glucose induced by lipotoxicity in major, high-mass high-energy tissues such as muscle without direct resupply of glucose portally (from meals). [/QUOTE]
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