Abstract
Background: Recent data show that atherosclerosis is initiated and perpetuated by inflammatory events. Activation of immune cells such as monocytes initiates inflammation, a key step in atherosclerosis. Objective: We hypothesize that a high-glycemic load meal activates inflammatory cells, and that this is mediated by elevated circulating triacylglycerol-rich lipoproteins. Design: Sixteen women [body mass index (in kg/m2): 25.7-29.6], aged 20-48 y, consumed meals with a high or a low glycemic load in a crossover fashion. Blood samples were collected before and up to 8 h after the meals. Samples were measured for glucose, insulin, triacylglycerols, and circulating cytokines, and expression of tumor necrosis factor α(TNF-α) and interleukin 1β (IL-1β) was measured by flow cytometry. Results: At 3.5 h after the test meals, we observed a significant increase in monocytes expressing TNF-α with both high- and low-glycemic load meals. Also, expression of IL-1β in monocytes tended to increase, but the change was not significant. The glycemic load of the meal did not influence circulating cytokines and had only a minimal effect on postprandial triacylglycerol concentrations despite marked postprandial changes in glycemia and circulating insulin concentrations. Conclusions: In the postprandial state, monocytes can be activated by both high- and low-glycemic load meals. The glycemic load of a single meal did not have a significant effect on the degree of activation of the monocytes in women who displayed only a modest increase in circulating triacylglycerols in response to test meals. Future studies should examine the effect of glycemic load in subjects who have a hyperlipemic response to dietary carbohydrate.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 60-65 |
| Number of pages | 6 |
| Journal | American Journal of Clinical Nutrition |
| Volume | 85 |
| Issue number | 1 |
| State | Published - Jan 1 2007 |
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Keywords
- Carbohydrates
- Glucose
- Glycemic index
- Inflammation
- Insulin
- Interleukin 6
- Monocytes
- Obesity
- Triacylglycerols
- Tumor necrosis factor α
ASJC Scopus subject areas
- Medicine (miscellaneous)
- Food Science
Cite this
Postprandial monocyte activation in response to meals with high and low glycemic loads in overweight women. / Motton, Deborah D.; Keim, Nancy L.; Tenorio, Fatima A.; Horn, William F.; Rutledge, John C.
In: American Journal of Clinical Nutrition, Vol. 85, No. 1, 01.01.2007, p. 60-65.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Postprandial monocyte activation in response to meals with high and low glycemic loads in overweight women
AU - Motton, Deborah D.
AU - Keim, Nancy L.
AU - Tenorio, Fatima A.
AU - Horn, William F.
AU - Rutledge, John C
PY - 2007/1/1
Y1 - 2007/1/1
N2 - Background: Recent data show that atherosclerosis is initiated and perpetuated by inflammatory events. Activation of immune cells such as monocytes initiates inflammation, a key step in atherosclerosis. Objective: We hypothesize that a high-glycemic load meal activates inflammatory cells, and that this is mediated by elevated circulating triacylglycerol-rich lipoproteins. Design: Sixteen women [body mass index (in kg/m2): 25.7-29.6], aged 20-48 y, consumed meals with a high or a low glycemic load in a crossover fashion. Blood samples were collected before and up to 8 h after the meals. Samples were measured for glucose, insulin, triacylglycerols, and circulating cytokines, and expression of tumor necrosis factor α(TNF-α) and interleukin 1β (IL-1β) was measured by flow cytometry. Results: At 3.5 h after the test meals, we observed a significant increase in monocytes expressing TNF-α with both high- and low-glycemic load meals. Also, expression of IL-1β in monocytes tended to increase, but the change was not significant. The glycemic load of the meal did not influence circulating cytokines and had only a minimal effect on postprandial triacylglycerol concentrations despite marked postprandial changes in glycemia and circulating insulin concentrations. Conclusions: In the postprandial state, monocytes can be activated by both high- and low-glycemic load meals. The glycemic load of a single meal did not have a significant effect on the degree of activation of the monocytes in women who displayed only a modest increase in circulating triacylglycerols in response to test meals. Future studies should examine the effect of glycemic load in subjects who have a hyperlipemic response to dietary carbohydrate.
AB - Background: Recent data show that atherosclerosis is initiated and perpetuated by inflammatory events. Activation of immune cells such as monocytes initiates inflammation, a key step in atherosclerosis. Objective: We hypothesize that a high-glycemic load meal activates inflammatory cells, and that this is mediated by elevated circulating triacylglycerol-rich lipoproteins. Design: Sixteen women [body mass index (in kg/m2): 25.7-29.6], aged 20-48 y, consumed meals with a high or a low glycemic load in a crossover fashion. Blood samples were collected before and up to 8 h after the meals. Samples were measured for glucose, insulin, triacylglycerols, and circulating cytokines, and expression of tumor necrosis factor α(TNF-α) and interleukin 1β (IL-1β) was measured by flow cytometry. Results: At 3.5 h after the test meals, we observed a significant increase in monocytes expressing TNF-α with both high- and low-glycemic load meals. Also, expression of IL-1β in monocytes tended to increase, but the change was not significant. The glycemic load of the meal did not influence circulating cytokines and had only a minimal effect on postprandial triacylglycerol concentrations despite marked postprandial changes in glycemia and circulating insulin concentrations. Conclusions: In the postprandial state, monocytes can be activated by both high- and low-glycemic load meals. The glycemic load of a single meal did not have a significant effect on the degree of activation of the monocytes in women who displayed only a modest increase in circulating triacylglycerols in response to test meals. Future studies should examine the effect of glycemic load in subjects who have a hyperlipemic response to dietary carbohydrate.
KW - Carbohydrates
KW - Glucose
KW - Glycemic index
KW - Inflammation
KW - Insulin
KW - Interleukin 6
KW - Monocytes
KW - Obesity
KW - Triacylglycerols
KW - Tumor necrosis factor α
UR - http://www.scopus.com/inward/record.url?scp=33846084836&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33846084836&partnerID=8YFLogxK
M3 - Article
C2 - 17209178
AN - SCOPUS:33846084836
VL - 85
SP - 60
EP - 65
JO - American Journal of Clinical Nutrition
JF - American Journal of Clinical Nutrition
SN - 0002-9165
IS - 1
ER -