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High fat intake leads to acute postprandial exposure to circulating endotoxin in type 2 diabetic subjects.

ABSTRACT: To evaluate the changes in circulating endotoxin after a high-saturated fat meal to determine whether these effects depend on metabolic disease state.Subjects (n = 54) were given a high-fat meal (75 g fat, 5 g carbohydrate, 6 g protein) after an overnight fast (nonobese control [NOC]: age 39.9 ± 11.8 years [mean ± SD], BMI 24.9 ± 3.2 kg/m(2), n = 9; obese: age 43.8 ± 9.5 years, BMI 33.3 ± 2.5 kg/m(2), n = 15; impaired glucose tolerance [IGT]: age 41.7 ± 11.3 years, BMI 32.0 ± 4.5 kg/m(2), n = 12; type 2 diabetic: age 45.4 ± 10.1 years, BMI 30.3 ± 4.5 kg/m(2), n = 18). Blood was collected before (0 h) and after the meal (1-4 h) for analysis.Baseline endotoxin was significantly higher in the type 2 diabetic and IGT subjects than in NOC subjects, with baseline circulating endotoxin levels 60.6% higher in type 2 diabetic subjects than in NOC subjects (P < 0.05). Ingestion of a high-fat meal led to a significant rise in endotoxin levels in type 2 diabetic, IGT, and obese subjects over the 4-h time period (P < 0.05). These findings also showed that, at 4 h after a meal, type 2 diabetic subjects had higher circulating endotoxin levels (125.4%?) than NOC subjects (P < 0.05).These studies have highlighted that exposure to a high-fat meal elevates circulating endotoxin irrespective of metabolic state, as early as 1 h after a meal. However, this increase is substantial in IGT and type 2 diabetic subjects, suggesting that metabolic endotoxinemia is exacerbated after high fat intake. In conclusion, our data suggest that, in a compromised metabolic state such as type 2 diabetes, a continual snacking routine will cumulatively promote their condition more rapidly than in other individuals because of the greater exposure to endotoxin.

SUBMITTER: Harte AL

PROVIDER: S-EPMC3263907 | biostudies-other | 2012 Feb

REPOSITORIES: biostudies-other

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High fat intake leads to acute postprandial exposure to circulating endotoxin in type 2 diabetic subjects.

Harte Alison L AL Varma Madhusudhan C MC Tripathi Gyanendra G McGee Kirsty C KC Al-Daghri Nasser M NM Al-Attas Omar S OS Sabico Shaun S O'Hare Joseph P JP Ceriello Antonio A Saravanan Ponnusamy P Kumar Sudhesh S McTernan Philip G PG

Diabetes care 20111230 2

<h4>Objective</h4>To evaluate the changes in circulating endotoxin after a high-saturated fat meal to determine whether these effects depend on metabolic disease state.<h4>Research design and methods</h4>Subjects (n = 54) were given a high-fat meal (75 g fat, 5 g carbohydrate, 6 g protein) after an overnight fast (nonobese control [NOC]: age 39.9 ± 11.8 years [mean ± SD], BMI 24.9 ± 3.2 kg/m(2), n = 9; obese: age 43.8 ± 9.5 years, BMI 33.3 ± 2.5 kg/m(2), n = 15; impaired glucose tolerance [IGT]: ...[more]

PMID: 22210577

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Project description:Background:Metabolic endotoxemia is associated with obesity and contributes to postprandial inflammation. Objective:We aimed to determine if low-fat yogurt consumption prevents postprandial inflammation and dysmetabolism in healthy women by inhibiting biomarkers of metabolic endotoxemia. Methods:Premenopausal women defined as obese and nonobese [body mass index (BMI, in kg/m2) 30-40 and 18.5-27, respectively, n = 120] were randomly assigned to consume 339 g of low-fat yogurt (YN, yogurt nonobese; YO, yogurt obese) or 324 g of soy pudding (CN, control nonobese; CO, control obese) for 9 wk (n = 30/group). The intervention foods each supplied 330 kcal with 3 g fat, 66 g carbohydrate, and 4-6 g protein. At weeks 0 and 9, participants ingested 226 g of yogurt or 216 g of soy pudding before a meal providing 56-60 g fat, 82 g carbohydrate, and 28-30 g protein. Plasma soluble CD14 (sCD14), lipopolysaccharide-binding protein (LBP), LPS activity, interleukin-6 (IL-6), glucose, triglyceride, and insulin were measured hourly for 4 h to assess differences in postprandial responses between groups by 2-factor ANOVA. Results:Premeal yogurt consumption prevented the postprandial decrease in sCD14 net incremental area under the curve (net iAUC) by 72% in obese individuals at week 0 (P = 0.0323). YN and YO had ?40% lower net iAUC of LBP-to-sCD14 ratio and plasma IL-6 concentration than CN and CO, respectively (P < 0.05). CO had postprandial hyperglycemia which was not evident in YO; in contrast YN had 57% less postprandial hypoglycemia than did CN (P-interaction = 0.0013). After 9 wk of yogurt consumption, ?AUC of LBP-to-sCD14 ratios of YO and YN were less than half of those of the control groups (P = 0.0093). Conclusion:Yogurt consumption improved postprandial metabolism and biomarkers of metabolic endotoxemia in healthy premenopausal women. Premeal yogurt consumption is a feasible strategy to inhibit postprandial dysmetabolism and thus may reduce cardiometabolic risk. This trial was registered at clinicaltrials.gov as NCT01686204.

Project description:High-fat diets may contribute to metabolic disease via postprandial changes in serum endotoxin and inflammation. It is unclear how dietary fat composition may alter these parameters. We hypothesized that a meal rich in n-3 (?3) fatty acids would reduce endotoxemia and associated inflammation but a saturated or n-6 (?6) fatty acid-rich meal would increase postprandial serum endotoxin concentrations and systemic inflammation in healthy adults.Healthy adults (n?=?20; mean age 25?±?3.2 S.D. years) were enrolled in this single-blind, randomized, cross-over study. Participants were randomized to treatment and reported to the laboratory, after an overnight fast, on four occasions separated by at least one week. Participants were blinded to treatment meal and consumed one of four isoenergetic meals that provided: 1) 20 % fat (control; olive oil) or 35 % fat provided from 2) n-3 (?3) (DHA?=?500 mg; fish oil); 3) n-6 (?6) (7.4 g; grapeseed oil) or 4) saturated fat (16 g; coconut oil). Baseline and postprandial blood samples were collected. Primary outcome was defined as the effect of treatment meal on postprandial endotoxemia. Serum was analyzed for metabolites, inflammatory markers, and endotoxin. Data from all 20 participants were analyzed using repeated-measures ANCOVA.Participant serum endotoxin concentration was increased during the postprandial period after the consumption of the saturated fat meal but decreased after the n-3 meal (p?<?0.05). The n-6 meal did not effect a different outcome in participant postprandial serum endotoxin concentration from that of the control meal (p?>?0.05). There was no treatment meal effect on participant postprandial serum biomarkers of inflammation. Postprandial serum triacylglycerols were significantly elevated following the n-6 meal compared to the n-3 meal. Non-esterified fatty acids were significantly increased after consumption of the saturated fat meal compared to other treatment meals.Meal fatty acid composition modulates postprandial serum endotoxin concentration in healthy adults. However, postprandial endotoxin was not associated with systemic inflammation in vivo.This study was retrospectively registered at clinicaltrials.gov as NCT02521779 on July 28, 2015.

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High fat intake leads to acute postprandial exposure to circulating endotoxin in type 2 diabetic subjects.

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High fat intake leads to acute postprandial exposure to circulating endotoxin in type 2 diabetic subjects.

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