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Abstract

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods and Procedures
  5. Results
  6. Discussion
  7. Acknowledgment
  8. Disclosure
  9. REFERENCES

The aim of this study was to compare the acute effect of (i) meals rich in saturated fat, oleic acid, and α-linolenic acid and (ii) meals rich in starch and fiber on markers of inflammation and oxidative stress in obese and lean women. In a crossover study, 15 abdominally obese women (age, 54 ± 9 years; BMI, 37.3 ± 5.5 kg/m2) and 14 lean women (age, 53 ± 10 years; BMI, 22.9 ± 1.9 kg/m2) consumed meals rich in cream (CR), olive oil (OL), canola oil (CAN), potato (POT), and All-Bran (BRAN) in random order. Blood samples were collected before and up to 6 h after the meals and plasma interleukin-6 (IL-6), IL-8, tumor necrosis factor-α (TNF-α), lipid peroxides (LPOs), free-fatty acids (FFAs), insulin, glucose, and cortisol were measured. Plasma IL-6 decreased significantly 1 h after the meals then increased significantly above baseline at 4 h and 6 h in obese women and at 6 h in lean women. The incremental area under the curve (iAUC) for IL-6 was significantly (P = 0.02) higher in obese compared with lean women and was significantly lower following the high fiber BRAN meal compared with a POT meal (P = 0.003). Waist circumference (R = 0.491, P = 0.007) and cortisol AUC (R = −0.415, P = 0.03) were significant determinants of the magnitude of 6 h changes in plasma IL-6 after the meals. These findings suggest that the postprandial response of plasma IL-6 concentrations may be influenced by the type of carbohydrate in the meal, central adiposity, and circulating cortisol concentrations in women.


Introduction

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods and Procedures
  5. Results
  6. Discussion
  7. Acknowledgment
  8. Disclosure
  9. REFERENCES

Obesity is associated with insulin resistance, glucose intolerance, and increased risk of type 2 diabetes and coronary heart disease. Adipocytes and/or associated macrophages can secrete a number of proteins termed adipokines, which affect insulin sensitivity and may provide a link between obesity and abnormalities in insulin action and glucose metabolism. Since interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and the chemokine IL-8 can be synthesized in adipose tissue (1), excess adipose tissue is thought to contribute to elevated circulating levels in obesity (2,3,4). These cytokines have been implicated in the development of insulin resistance. Infusion of TNF-α impairs skeletal muscle insulin signaling and decreases whole-body glucose uptake in healthy humans (5). Also there is evidence that IL-6 impairs hepatic insulin action (6). In the obese, plasma IL-8 concentrations are correlated inversely with insulin sensitivity (7) and higher levels of proinflammatory mediators are linked to lower insulin receptor phosphorylation in mononuclear cells that is consistent with impaired insulin action (8).

Dietary saturated fat impairs insulin action and glucose metabolism (9), whereas dietary unsaturated fats have the opposite effect (10). Saturated fat in the form of palmitic acid induces inflammation with increased expression and/or secretion of IL-6 or TNF-α in cultured adipocytes (11), muscle cells (12), and adipose tissue macrophages (13). In contrast, the n−3 fatty acid α-linolenic acid has anti-inflammatory activity (14) and inhibits expression and secretion of IL-6 from cultured human monocytes (15). There is evidence that ingestion of fatty meals may acutely modulate circulating concentrations of adipokines (16,17,18,19,20) and insulin resistance (21). In obese subjects, plasma IL-6 concentrations increase during 2–4 h after a liquid meal rich in saturated and monounsaturated fats (18). However, the effect of obesity and the type of fat in the meal on postprandial adipokine concentrations is not yet clearly defined.

There is evidence that intake of carbohydrate and fiber also modulates inflammation. A meal high in both carbohydrate and fiber decreases while a meal high in carbohydrate and low in fiber does not alter plasma concentrations of the proinflammatory cytokine IL-18 appreciably (17). Few studies have investigated the acute effect of meals rich in different types of fatty acids and rich in low glycemic index (GI) high fiber cereals on postprandial adipokine levels in obese individuals. The aim of the present study was therefore to compare the effect of meals consisting of potato starch with or without added canola oil, olive oil, and cream and a meal containing low GI, high fiber cereal on postprandial concentrations of plasma IL-6, TNF-α, and IL-8 in obese and nonobese women.

Methods and Procedures

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods and Procedures
  5. Results
  6. Discussion
  7. Acknowledgment
  8. Disclosure
  9. REFERENCES

Subjects

We recruited 20 healthy women with BMI >30 kg/m2 and waist circumference ≥88 cm and 15 women with BMI 20–25 kg/m2 and waist circumference <88 cm in the age range 30–70 years. Subjects were recruited from respondents to a newspaper advertisement and from subjects who participated in earlier studies we have conducted and indicated they would be available for future studies. Exclusion criteria included pregnancy, cigarette smoking, history of cardiovascular disease, and other serious illnesses, current infection, and use of medications including hormone replacement therapy but not the contraceptive pill. Women with the features of the metabolic syndrome including hypertension and dyslipidemia were not excluded. Participants gave informed and written consent and the study was approved by the Lower South Regional Ethics Committee.

Study design

The study had a single-blind, randomized, crossover design. Participants were randomly assigned to a sequence of the five test meals with at least a week between each meal using the mutually orthogonal Latin Squares method on the www.ams.orgnew-in-mathcoverlatinII3.html website. After an overnight fast, participants reported to the study center in the early morning (∼8:00 am). A venous blood sample was taken and a meal was immediately consumed within 15 min. Blood samples were taken at 1 h, 4 h, and 6 h after consumption of the meal. Participants were allowed to consume water but not other beverages and food and they remained seated during the study. Subjects were instructed to maintain their usual lifestyle in the periods between the meals. Anthropometric measurements were made before each meal and blood pressure was measured at baseline.

Meals

The potato (POT), cream (CR), olive oil (OL), and canola oil (CAN) meals all contained 200 g instant mash potato (Cinderella) and two eggs that had been cooked by microwave. The CR meal contained 1.6 g cream/kg body weight and the instant potato was reconstituted with 100 ml of hot water. The OL and CAN meals contained 0.6 g/kg body weight of olive oil and canola oil, respectively, and the instant potato was reconstituted with 160 ml hot water. The instant potato in the POT meal was also reconstituted with 160 ml hot water. The BRAN meal contained All-Bran, trim milk (40 ml), and two cooked eggs. The nutrient composition of the meals is shown in Table 1. The composition of the meals was analyzed using the USDA National Nutrient Database for Standard Reference (http:grande.nal.usda.gov) and the Foods Standards Australia and New Zealand Database (www.foodstandards.gov.au). The α-linolenic acid content of test fats were estimated using published data (22). The GI of All-Bran is 42 and is 88 for mash potato.

Table 1.  Composition of the meals in obese and lean women
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Laboratory methods

Venous blood was taken into tubes containing EDTA and into plain tubes. Serum and EDTA plasma were prepared by centrifugation of the tubes at 1,500g for 15 min at 4 °C. Aliquots of serum and plasma were harvested and stored at −80 °C. Plasma glucose was measured by routine automated methods in the Otago Diagnostic Laboratories, Dunedin Hospital. Plasma insulin and C-reactive protein were measured on a Hitachi 911 autoanalyser using commercial kits and calibrators (Roche Diagnostic, Mannheim, Germany). Serum cortisol was measured using a routine immunological method in the laboratories of the Endocrinology Service, Christchurch Hospital, Christchurch, New Zealand. High-density lipoprotein (HDL) cholesterol was measured in the plasma supernatant after precipitation of apolipoprotein B-containing lipoproteins (23). Plasma lipids and lipoprotein lipids were measured by routine automated methods using commercial kits and calibrators (Roche Diagnostics, Mannheim, Germany). Plasma free-fatty acid (FFA) concentrations were measured using a commercial kit (Roche Diagnostics, Mannheim, Germany). The concentration of lipid peroxides (LPOs) in plasma was measured, as was previously described (24), with an incubation time of 45 min. This method is based on the cleavage of LPOs by horseradish peroxidase, leading to oxidation of tetramethylbenzidine to a colored compound that can be measured spectrophotometrically. Plasma IL-6 and TNF-α were measured by high sensitivity enzyme-linked immunosorbent assay methods using commercial kits (R&D Systems, Minneapolis, MN). The intraassay coefficients of variation for these assays were 7 and 8%, respectively. IL-8 was also measured in duplicate by a modified enzyme-linked immunosorbent assay method using a commercial kit (R&D Systems, Minneapolis, MN). The assay was modified by using a lower IL-8 standard, increasing the length of time allowed for the absorption of plasma IL-8 onto the plate, and increasing the number of washes of the plate to remove nonspecifically absorbed plasma material. All the cytokines were measured in duplicate and assays used dual wavelength spectrophotometry. Samples from an individual were measured in the same assay to reduced interassay variation for IL-6, IL-8, TNF-α, insulin, C-reactive protein, FFA, and LPO.

Statistics

Values are given as mean ± s.d. unless stated otherwise. The trapezium method was used to calculate incremental area under the curve (iAUC) and area under the curve (AUC) (25). Friedman's nonparametric repeated measures ANOVA was used to compare iAUC values for variables among the fatty meals (CR, OL, and CAN) in obese and lean women separately. If a significant difference in ANOVA was detected, then values for individual meals were compared by Wilcoxon's signed rank test. Wilcoxon's signed rank test was also used to separately compare iAUC values for variables between the carbohydrate meals (BRAN and POT). The Mann-Whitney test was used to compare baseline values and the mean iAUC of a variable for all meals in each individual, between obese and lean women. Parametric repeated measures ANOVA on log-transformed data was used to analyze changes in variables with time and to estimate carryover by comparing zero-time values before the meals. There was no evidence of significant carryover in the data. Linear regression analysis was used to predict 6 h changes in plasma IL-6 concentrations. Two-sided test of significance was used and a P value of <0.05 was considered to be statistically significant.

Results

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods and Procedures
  5. Results
  6. Discussion
  7. Acknowledgment
  8. Disclosure
  9. REFERENCES

Characteristics of the subjects

Five obese women and one lean woman withdrew from the study after the first or second meal because they could not tolerate the meals or venipuncture (one). Table 2 summarizes the characteristics of the remaining participants. The obese women had higher blood pressure and fasting concentrations of plasma insulin, glucose, C-reactive protein, IL-6, TNF-α, and LPO and lower concentrations of serum cortisol and plasma HDL cholesterol compared with lean women. Two women, both lean, were taking the oral contraceptive pill. Body weight (P = 0.83) and waist circumference (P = 0.29) did not change significantly during the study.

Table 2.  Characteristics of the obese and lean women at baseline
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Glucose, insulin, and blood lipids

Figure 1 shows plasma glucose, insulin, triglyceride (TG), and HDL cholesterol concentrations after the meals. Plasma glucose concentration increased significantly 1 h after the POT and OL meals and at a marginal level of significance (P = 0.05) after the BRAN meal in obese women and did not change significantly in lean women. At 4 h and 6 h after the meals, plasma glucose concentration was significantly lower than baseline in obese women. Plasma insulin concentration increased significantly at 1 h and was significantly lower than baseline at 6 h after all meals in obese and lean women. In obese women, plasma TG concentrations increased significantly 4 h after all meals and remained significantly higher than baseline at 6 h after all fatty meals. In lean women, plasma TG concentrations were significantly higher than baseline after all meals excepting the POT meal and remained significantly higher than baseline 6 h after the OL and CAN meals. There were small (2–4%), significant increases in plasma HDL cholesterol concentration from baseline at 6 h mainly due to increases during the BRAN and POT meals in obese women and following the OL meal in lean women. Plasma total cholesterol concentration did not change significantly after the meals (data not shown). Plasma glucose, insulin, and HDL cholesterol iAUCs were not significantly different among the fatty meals and between the BRAN meal and the POT meal in obese and lean women. The iAUC of plasma TG was significantly (P = 0.009) lower following the CAN meal compared with the CR meal in obese women and was significantly higher after the BRAN meal compared with the POT meal in obese (P = 0.03) and lean (P = 0.002) women. The postprandial iAUCs of glucose, insulin, TG, and HDL cholesterol were not significantly different between obese and lean women.

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Figure 1. Concentration and incremental area under curve (iAUC) for plasma (a) glucose, (b) insulin, (c) triglyceride (TG), and (d) high-density lipoprotein cholesterol (HDL-C) in obese and lean women. Abbreviations: CR, cream; OL, olive oil; CAN, canola oil; BRAN, All-Bran; POT, potato. Obese: open bars; lean: filled bars in the iAUC panel of the figure. Meals obese women: CR, open squares; OL, open diamonds; CAN, open circles; BRAN, open inverted triangles; POT, open triangles. Meals lean women: CR, filled squares; OL, filled diamonds; CAN, filled circles; BRAN, filled inverted triangles; POT, filled triangles. Significance of comparison of iAUC among the fatty meals (Pfats) and carbohydrate meals (Pcarb):*P < 0.05, P = 0.002, P = 0.009 between individual meals. Significantly different from baseline: aP < 0.05 POT and OL meals in obese women; bP < 0.01 all meals in obese women; cP ≤ 0.001 all meals in all women; dP < 0.05 OL and BRAN in obese women and CAN, BRAN, and POT in lean women; eP ≤ 0.001 CR, OL, and BRAN in all women, and POT in obese women; fP < 0.001 all meals in obese women and all but POT meal in lean women; gP < 0.001 CR, OL, CAN meals in obese women and P < 0.05 OL, CAN in lean women.

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Cytokines and FFA

Figure 2 shows plasma concentrations of cytokines and FFA in the women during the postprandial period after the meals. Plasma IL-6 decreased significantly at 1 h then increased to become significantly higher than baseline at 4 h in obese women and at 6 h in both obese and lean women. After the BRAN meal compared with the POT meal, the iAUC for plasma IL-6 was significantly lower in lean women (P = 0.02) and was lower at a marginal level of significance in obese women (P = 0.06). Plasma IL-6 iAUC did not differ significantly among the fatty meals in obese (P = 0.98) and lean (P = 0.75) women. In obese women, plasma IL-6 iAUC was not significantly different between the POT meal and the CR (P = 0.40), OL (P = 0.11), and CAN (P = 0.36) meals. Plasma IL-6 iAUC was significantly higher in obese compared with lean women during the meals. Plasma TNF-α and IL-8 concentrations did not change significantly during the meals. The iAUC plasma TNF-α was significantly lower during the BRAN compared with the POT meal in obese women. The time course of plasma FFA concentrations after the meals essentially paralleled the corresponding time course of plasma IL-6 with a significant decrease at 1 h and significant increases at 4 h and 6 h in both obese and lean women. The iAUCs for plasma TNF-α, IL-8, and FFA concentrations were not significantly different between obese and lean women during the meals.

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Figure 2. Concentration and incremental area under curve (iAUC) for (a) plasma interleukin-6 (IL-6), (b) tumor necrosis factor-α (TNF-α), (c) free-fatty acids (FFA), and (d) interleukin-8 (IL-8) in obese and lean women. Abbreviations: CR, cream; OL, olive oil; CAN, canola oil; BRAN, All-Bran; POT, potato. Obese: open bars; lean: filled bars in the iAUC panel of the figure. Meals obese women: CR, open squares; OL, open diamonds; CAN, open circles; BRAN, open inverted triangles; POT, open triangles. Meals lean women: CR, filled squares; OL, filled diamonds; CAN, filled circles; BRAN, filled inverted triangles; POT, filled triangles. Significance of comparison of iAUC among the fatty meals (Pfats) and carbohydrate meals (Pcarb): *P = 0.06, P < 0.05 between individual meals. Significantly different from baseline: aP < 0.05 CAN, BRAN, and POT meals in obese women and CR, OL, BRAN, and POT meals in lean women; bP < 0.01 CR, OL, and POT meals in obese women; cP < 0.01 all meals in obese women and P < 0.05 POT meal in lean women; dP < 0.05 CR, CAN, BRAN, and POT meals in obese women and all meals in lean women; eP < 0.05 CAN, BRAN, and POT meals in obese women and CR, OL, and BRAN in lean women; fP < 0.05 all meals in all women.

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Cortisol and LPO

Figure 3 shows serum cortisol and LPO concentrations after the meals. Serum cortisol concentrations decreased significantly from baseline following the meals and were significantly (P = 0.02, repeated measures ANOVA with obesity as a between subjects factor) lower in obese women compared with lean women during the meals. The cortisol iAUC was not significantly different among the meals and tended (P = 0.06) to be larger in lean compared with obese women. Plasma LPO concentrations did not vary significantly after the meals.

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Figure 3. Concentration and incremental area under curves (iAUC) for (a) plasma lipid peroxides (LPOs) and (b) serum cortisol. Abbreviations: CR, cream; OL, olive oil; CAN, canola oil; BRAN, All-Bran; POT, potato. Obese: open bars; lean: filled bars in the iAUC panel of the figure. The iAUCs for fatty meals and carbohydrate meals were compared separately. Meals obese women: CR, open squares; OL, open diamonds; CAN, open circles; BRAN, open inverted triangles; POT, open triangles. Meals lean women: CR, filled squares; OL, filled diamonds; CAN, filled circles; BRAN, filled inverted triangles; POT, filled triangles. Significantly different from baseline: aP < 0.05 all meals in all women; bP < 0.01 all meals in all women.

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Regression analyses

Figure 4 shows representative relationships between the 6 h change in plasma IL-6 concentrations and waist circumference and AUC cortisol after the meals in the total study population. Waist circumference (R = 0.353 to 0.496, P ≤ 0.01 for all but the OL meal for which P = 0.07) and AUC cortisol (R = −0.291 to −0.520, P < 0.05 CR, POT, and BRAN meals) were significant determinants of the 6 h increase in plasma IL-6 concentration during most of the meals. Plasma FFA concentrations were not a significant determinant of plasma IL-6 concentrations after the meals (data not shown).

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Figure 4. Relationships between the 6 h change in plasma interleukin-6 (IL-6) concentrations and (a) waist circumference and (b) area under the curve (AUC) of serum cortisol concentrations during a meal. Obese (open squares) and lean (open diamonds) women.

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Discussion

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods and Procedures
  5. Results
  6. Discussion
  7. Acknowledgment
  8. Disclosure
  9. REFERENCES

The results of the present study indicate that plasma IL-6 concentrations increased to levels substantially above baseline in the late postprandial period after meals rich in high GI carbohydrate with and without fat and after ingestion of low GI, high fiber carbohydrate. This response of plasma IL-6 to the meals was markedly higher in obese compared with lean women and was lower after ingestion of low GI, high fiber carbohydrate compared with high GI, low fiber carbohydrate. The type of fat in the meal did not have an appreciable effect.

Our findings are in keeping with previous studies that have reported a substantial increase in plasma IL-6 concentrations during 4 h after a liquid meal rich in saturated and monounsaturated fats (18) and a prolonged postprandial inflammatory response after a high-fat, high-carbohydrate meal in obese individuals (26). We now extend these data to show that obesity enhances the postprandial increase in plasma IL-6 in women irrespective of the type or content of fat in the meal and that meals rich in fiber attenuate this increase in IL-6.

Ingestion of meals rich in fiber may acutely reduce inflammatory activity (17). The mechanism responsible for this anti-inflammatory effect of dietary fiber has not been elucidated but might involve enhanced antioxidant activity (17) and/or an intestinal anti-inflammatory effect (27). In the present study, the reduced total response of plasma IL-6, as indicated by lower iAUC, to the fiber-rich BRAN meal compared with the high carbohydrate, low fiber POT meal would appear to be in keeping with an anti-inflammatory effect of dietary fiber. However, this response to a meal rich in fiber did not appear to be mediated by change in oxidative stress since plasma LPO concentrations did not vary appreciably after the meals. Plasma LPO concentration is a marker of systemic oxidative stress and higher levels in the obese women confirms previous reports of increased oxidative stress in obesity (28,29).

There is evidence that saturated fats are proinflammatory and oleic acid and α-linolenic acid are anti-inflammatory (11,12,13,14,15). Ingestion of saturated fats, such as cream, may increase inflammatory activity and plasma IL-6 by increasing the generation of reactive oxygen species that are known to upregulate nuclear transcription factor-κB mediated inflammation (18,30,31). However, our results suggest that the type of fat in a mixed meal does not acutely influence inflammatory status in obese and lean women. The magnitude of the postprandial increase in plasma IL-6 was similar after meals rich in saturated fatty acids, oleic acid, and α-linolenic acid. Furthermore, there was no evidence of an acute proinflammatory effect of ingested saturated fat. The postprandial increase in plasma IL-6 concentration was not augmented when cream was added to the POT meal. It is possible that the postprandial increase in insulin levels may have attenuated the generation of reactive oxygen species and inflammation after the meals rich in fat and potato. Plasma LPO concentrations did not vary appreciably after the meals. Also plasma IL-6 decreased temporarily 1 h following the meals suggesting a decrease in inflammatory activity when insulin levels were high. Dandona and co-workers have previously shown that insulin has anti-inflammatory and antioxidant properties and have postulated that postprandial hyperinsulinemia may potentially counteract acute inflammatory stress of macronutrient intake (32,33).

Plasma TNF-α concentrations did not increase in parallel with plasma IL-6 concentrations in obese women after the meals in the current study. It is possible that plasma TNF-α concentrations do not reflect closely adipose tissue TNF-α content. Mohamed-Ali and co-workers have reported that human subcutaneous adipose tissue does not release TNF-α in vivo (2).

Our data suggest that excess adipose tissue and low plasma cortisol concentrations may contribute to the enhanced increase in plasma IL-6 concentrations in obese women after meals rich in fat and carbohydrate. Central adiposity, as measured by waist circumference, predicted the magnitude of the 6 h increase in plasma IL-6 after the meals. Previous studies suggest that excess adipose tissue may contribute substantially to abnormally high plasma IL-6 concentrations in the obese. Adipose tissue content of IL-6 is approximately fourfold higher in obese compared with lean individuals and correlates with plasma IL-6 concentrations (3). Furthermore, there is evidence that IL-6 contributes up to 30% of circulating IL-6 in nonobese individuals (2). During the postprandial period after a meal, IL-6 increases markedly in the interstitial fluid of subcutaneous adipose tissue (34) and this may increase plasma concentrations. Increased accumulation of macrophages (35) may contribute to increased inflammatory activity and IL-6 content of adipose tissue in obese individuals.

Endogenous cortisol can inhibit production of inflammatory cytokines TNF-α, IL-1, and IL-6 (36) and is an important component of the endogenous anti-inflammatory system. In the present study, lower AUC serum cortisol predicted a larger increase in plasma IL-6 after the meals. This finding is consistent with the anti-inflammatory action of cortisol. The decrease in serum cortisol after the meals was not affected appreciably by the type of meal consumed and was probably due mainly to diurnal variation. Serum cortisol concentrations show considerable diurnal variation and early morning levels decrease markedly from 8:00 am to 1:00 pm (37). Abnormally low serum cortisol concentration in obese women has been reported previously (38).

This study has limitations. The number of participants was relatively small and did not include men. Thus caution must be exercised in the extrapolation of findings to larger populations. Obese women ingested more fat during the fatty meals in proportion with their higher body weight compared with lean women. However, it is unlikely that higher fat intake was responsible for the larger response of plasma IL-6 to meals in obese compared with lean women. Plasma IL-6 iAUC was clearly higher in obese compared with lean women after the BRAN and POT meals that contained relatively low amounts of fat. Also, in obese women, the iAUC of plasma IL-6 was not appreciably different between the fatty meals and the BRAN meal that contained markedly less fat. Our study design did not take into account the menstrual cycle and timing of oral contraceptive usage in the women.

In conclusion, these data suggest that the type of carbohydrate consumed, central adiposity, and circulating cortisol concentrations are determinants of the magnitude of postprandial plasma IL-6 response to meals. Furthermore, neither the type nor quantity of fat in the meal appears to influence this response. The exaggerated increase in plasma IL-6 after meals in obese women may be due to expanded fat mass with enhanced inflammatory activity in adipose tissue as a result of large adipocytes and low levels of cortisol-mediated endogenous anti-inflammatory activity. Further studies are needed to clarify the physiological impact of exaggerated postprandial increases in plasma IL-6 in obese women.

Acknowledgment

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods and Procedures
  5. Results
  6. Discussion
  7. Acknowledgment
  8. Disclosure
  9. REFERENCES

The authors are grateful to the participants in the study. This study was supported by a grant from the National Heart Foundation of New Zealand.

REFERENCES

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods and Procedures
  5. Results
  6. Discussion
  7. Acknowledgment
  8. Disclosure
  9. REFERENCES
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