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The study tested high carb diets combined with either palmitic acid (not from a natural source) or high oleic acid sunflower oil (7.6:1 ratio for MUFA:PUFA).
Specific Macronutrients Exert Unique Influences on the Adipose-Liver Axis to Promote Hepatic Steatosis in Mice
"only mice fed starch-enriched diets displayed hyperinsulinemia at 6 months (Table 2), and only those fed starch-oleate exhibited glucose intolerance"
"Mice fed starch-oleate displayed the worst steatosis, accumulating at least 40% more hepatic lipid than the other 3 high-energy diet groups (Figure 2D and E). Starch-oleate–fed mice also showed more evidence of liver injury than did mice in the other high-energy groups. "
Sucrose-oleate was actually less harmful than the starch-oleate.
"Viewing these results together with the stable isotope incorporation data, it is evident that DNL and adipose tissue lipolysis both contribute to hepatic steatosis in response to high-energy diets but adipose tissue lipolysis is disproportionately increased in response to a starch-oleate diet."
Interestingly, the increase in lipolysis was only found in the starch-oleate group and not the sucrose-oleate group.
"The data demonstrate that a monounsaturated fat-enriched diet provokes more hepatic steatosis than a saturated fat-enriched diet, particularly when combined with a complex CHO such as starch."
"our experiments demonstrated that starch-oleate feeding actually induced progressive necrosis of adipose tissue. The downstream consequence of this adipose tissue involution was worsening of hepatic steatosis."
So the starch-oleate not only promoted liver dysfunction, but also adipose tissue dysfunction. This leads to high inflammation, less fat storage, insulin resistance, glucose intolerance, etc.
"studies in humans demonstrate that accumulation of unsaturated fatty acids in adipose tissue is associated with insulin resistance, reduced DNL, and enhanced lipolysis.45, 46 Thus, oleate loading of adipocytes appears to be an important trigger to a decline in adipose tissue mass with resultant hepatic steatosis."
Specific Macronutrients Exert Unique Influences on the Adipose-Liver Axis to Promote Hepatic Steatosis in Mice
"only mice fed starch-enriched diets displayed hyperinsulinemia at 6 months (Table 2), and only those fed starch-oleate exhibited glucose intolerance"
"Mice fed starch-oleate displayed the worst steatosis, accumulating at least 40% more hepatic lipid than the other 3 high-energy diet groups (Figure 2D and E). Starch-oleate–fed mice also showed more evidence of liver injury than did mice in the other high-energy groups. "
Sucrose-oleate was actually less harmful than the starch-oleate.
"Viewing these results together with the stable isotope incorporation data, it is evident that DNL and adipose tissue lipolysis both contribute to hepatic steatosis in response to high-energy diets but adipose tissue lipolysis is disproportionately increased in response to a starch-oleate diet."
Interestingly, the increase in lipolysis was only found in the starch-oleate group and not the sucrose-oleate group.
"The data demonstrate that a monounsaturated fat-enriched diet provokes more hepatic steatosis than a saturated fat-enriched diet, particularly when combined with a complex CHO such as starch."
"our experiments demonstrated that starch-oleate feeding actually induced progressive necrosis of adipose tissue. The downstream consequence of this adipose tissue involution was worsening of hepatic steatosis."
So the starch-oleate not only promoted liver dysfunction, but also adipose tissue dysfunction. This leads to high inflammation, less fat storage, insulin resistance, glucose intolerance, etc.
"studies in humans demonstrate that accumulation of unsaturated fatty acids in adipose tissue is associated with insulin resistance, reduced DNL, and enhanced lipolysis.45, 46 Thus, oleate loading of adipocytes appears to be an important trigger to a decline in adipose tissue mass with resultant hepatic steatosis."