Fructose augments synthesis and release of free fatty acids and lactate

JCastro

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Metabolic fate of fructose in human adipocytes: a targeted 13C tracer fate association study

”This study demonstrated that fructose stimulates anabolic processes in adipocytes robustly, including glutamate and de novo fatty acid synthesis. Furthermore, fructose also augments the release of free palmitate from fully differentiated adipocytes. These results imply that in the presence of fructose, the metabolic response of adipocytes in culture is altered in a dose dependent manner, particularly favoring increased glutamate and fatty acid synthesis and release

Fructose robustly increased intracellular palmitate, de novo palmitate synthesis and the release of palmitate from adipocytes

A 1.5–2.0-fold increase in the release of labeled palmitate from fully differentiated adipocytes was observed in cells treated with 2.5–10 mM fructose as compared to the 0.1 mM fructose treated group (i.e., the control). Overall, fructose increased intracellular palmitate formation in a robust manner in fully differentiated adipocytes while simultaneously also increasing the release of palmitate from the cells.

”fructose-treated adipocytes also demonstrated an increase in the accumulation of intracellular oleate in differentiating and differentiated adipocytes ... Oleate is formed by the elongation and desaturation of palmitate. These results imply that in addition to the activity of fatty acid synthase, fructose also increases the action of fatty acid elongase and fatty acid desaturase to bring about the conversion of palmitate to oleate thus promoting the storage of fatty acids as both oleate and palmitate.“

“Fructose augmented acetyl-CoA formation and lactate release in adipocytes

Examining the [13C]-lactate in the extracellular medium revealed that fully differentiated adipocytes but not differentiating adipocytes, showed show a dose-dependent release of lactate into the extracellular medium. The release was robust only at the higher concentrations of fructose (5, 7.5 and 10 mM) in differentiated adipocytes, suggesting that adipocytes efficiently produced lactate only in the presence of excess fructose.”

There is also an attempt by the cell to simultaneously replenish the palmitate pool in the presence of increasing fructose concentrations as palmitate formed is being used up either for conversion to stearate and subsequently oleate or for release from adipocytes

fructose was used as a substrate for oxidation in differentiating adipocytes but the primary use of fructose in differentiated adipocyte is for anabolic processes such as synthesis of fatty acids and non-essential amino acids.

a 4.33-fold increase in fatty acid synthase and (iii) a resulting 4.8-fold increase in the fatty acid palmitate synthesized from fructose. A 2.56-fold increase was also seen in the formation of oleate. Although fatty acids, palmitate, and oleate were formed in response to fructose, only palmitate was released from the cells, a process augmented by 1.67-fold in presence of 5 mM fructose."
 

Kvothe

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Metabolic fate of fructose in human adipocytes: a targeted 13C tracer fate association study

”This study demonstrated that fructose stimulates anabolic processes in adipocytes robustly, including glutamate and de novo fatty acid synthesis. Furthermore, fructose also augments the release of free palmitate from fully differentiated adipocytes. These results imply that in the presence of fructose, the metabolic response of adipocytes in culture is altered in a dose dependent manner, particularly favoring increased glutamate and fatty acid synthesis and release

Fructose robustly increased intracellular palmitate, de novo palmitate synthesis and the release of palmitate from adipocytes

A 1.5–2.0-fold increase in the release of labeled palmitate from fully differentiated adipocytes was observed in cells treated with 2.5–10 mM fructose as compared to the 0.1 mM fructose treated group (i.e., the control). Overall, fructose increased intracellular palmitate formation in a robust manner in fully differentiated adipocytes while simultaneously also increasing the release of palmitate from the cells.

”fructose-treated adipocytes also demonstrated an increase in the accumulation of intracellular oleate in differentiating and differentiated adipocytes ... Oleate is formed by the elongation and desaturation of palmitate. These results imply that in addition to the activity of fatty acid synthase, fructose also increases the action of fatty acid elongase and fatty acid desaturase to bring about the conversion of palmitate to oleate thus promoting the storage of fatty acids as both oleate and palmitate.“

“Fructose augmented acetyl-CoA formation and lactate release in adipocytes

Examining the [13C]-lactate in the extracellular medium revealed that fully differentiated adipocytes but not differentiating adipocytes, showed show a dose-dependent release of lactate into the extracellular medium. The release was robust only at the higher concentrations of fructose (5, 7.5 and 10 mM) in differentiated adipocytes, suggesting that adipocytes efficiently produced lactate only in the presence of excess fructose.”

There is also an attempt by the cell to simultaneously replenish the palmitate pool in the presence of increasing fructose concentrations as palmitate formed is being used up either for conversion to stearate and subsequently oleate or for release from adipocytes

fructose was used as a substrate for oxidation in differentiating adipocytes but the primary use of fructose in differentiated adipocyte is for anabolic processes such as synthesis of fatty acids and non-essential amino acids.

a 4.33-fold increase in fatty acid synthase and (iii) a resulting 4.8-fold increase in the fatty acid palmitate synthesized from fructose. A 2.56-fold increase was also seen in the formation of oleate. Although fatty acids, palmitate, and oleate were formed in response to fructose, only palmitate was released from the cells, a process augmented by 1.67-fold in presence of 5 mM fructose."
1. This is an in vitro study with isolated adipocytes. Doesn't really tell you anthing about what happens when a person metabolizes sugar.
2. Did they treat cells with the same amount of glucose as a control?
3. What exactely do you expect will happen when you feed isolated fat cells increasing amounts of substrate that has to go somewhere?
 
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