Postprandial energy metabolism and substrate #oxidation in response to the inclusion of a sugar- or non-nutritive #sweetened beverage with meals differing in protein content
https://bmcnutr.biomedcentral.com/articles/10.1186/s40795-017-0170-2
The observed increase in dietary carbohydrates has come primarily from added sugars, accounting for approximately 16%E of total energy intake. The largest single source of added sugar and discretionary energy intake in the American diet is sugar-sweetened beverages (SSBs) In addition to increasing energy intake, SSBs may significantly affect postprandial fat oxidation. Stookey et al. recently reported that the addition of orange juice with a standard breakfast meal decreased fat oxidation compared to the same meal coupled with water This acute effect on net fat oxidation leads to preferential increases in visceral adipose tissue when consumed daily over long periods
Taken together, these results suggest that the consumption of SSBs may be contributing to weight gain by adding energy to the diet and reducing fat oxidation This work adds to the mounting evidence that SSB consumption can increase an individual’s susceptibility to weight gain and fat accumulation, especially when paired with a higher protein meal. These data highlight the need to design strategies aimed at maximizing macronutrient balance instead of focusing on interventions that strictly target energy balance
https://bmcnutr.biomedcentral.com/articles/10.1186/s40795-017-0170-2
The observed increase in dietary carbohydrates has come primarily from added sugars, accounting for approximately 16%E of total energy intake. The largest single source of added sugar and discretionary energy intake in the American diet is sugar-sweetened beverages (SSBs) In addition to increasing energy intake, SSBs may significantly affect postprandial fat oxidation. Stookey et al. recently reported that the addition of orange juice with a standard breakfast meal decreased fat oxidation compared to the same meal coupled with water This acute effect on net fat oxidation leads to preferential increases in visceral adipose tissue when consumed daily over long periods
Taken together, these results suggest that the consumption of SSBs may be contributing to weight gain by adding energy to the diet and reducing fat oxidation This work adds to the mounting evidence that SSB consumption can increase an individual’s susceptibility to weight gain and fat accumulation, especially when paired with a higher protein meal. These data highlight the need to design strategies aimed at maximizing macronutrient balance instead of focusing on interventions that strictly target energy balance
BioMed Central
Postprandial energy metabolism and substrate oxidation in response to the inclusion of a sugar- or non-nutritive sweetened beverage…
Background The macronutrient composition of the diet may play a more important role in maintaining a healthy body weight and preventing obesity than previously thought. The primary goal of this research was to determine the extent to which the simple addition…
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Dietary #Sugars Alter Hepatic #Fatty Acid #Oxidation via Transcriptional and Post-translational Modifications of Mitochondrial Proteins
Highlights
• Addition of fructose to a high-fat diet increases hepatic malonyl-CoA more than glucose
•Knockdown of the fructose metabolizing gene ketohexokinase increases CTP1a levels
•Fructose supplementation alters mitochondrial size and function
•Dietary fructose induces acetylation of ACADL and CPT1a to modify fat oxidation
In summary, dietary fructose, but not glucose, supplementation of HFD impairs mitochondrial size, function, and protein acetylation, resulting in decreased fatty acid oxidation and development of metabolic dysregulation.
https://www.cell.com/cell-metabolism/fulltext/S1550-4131(19)30504-2
Dietary #Sugars Alter Hepatic #Fatty Acid #Oxidation via Transcriptional and Post-translational Modifications of Mitochondrial Proteins
Highlights
• Addition of fructose to a high-fat diet increases hepatic malonyl-CoA more than glucose
•Knockdown of the fructose metabolizing gene ketohexokinase increases CTP1a levels
•Fructose supplementation alters mitochondrial size and function
•Dietary fructose induces acetylation of ACADL and CPT1a to modify fat oxidation
In summary, dietary fructose, but not glucose, supplementation of HFD impairs mitochondrial size, function, and protein acetylation, resulting in decreased fatty acid oxidation and development of metabolic dysregulation.
https://www.cell.com/cell-metabolism/fulltext/S1550-4131(19)30504-2