High fat intake leads to acute postprandial exposure to circulating endotoxin in type 2 diabetic subjects
Harte, A. L. (Alison L.), Varma, Madhusudhan C., Tripathi, G. N. (Gyanendra Nath), 1933-, McGee, K. C. (Kirsty Claire), Al-Daghri, Nasser M., Al-Attas, Omar S., Sabico, Shaun, O'Hare, J. Paul, Ceriello, Antonio, Saravanan, Ponnusamy, Kumar, Sudhesh and McTernan, P. G. (Philip G.). (2012) High fat intake leads to acute postprandial exposure to circulating endotoxin in type 2 diabetic subjects. Diabetes Care, Vol.35 (No.2). pp. 375-382. ISSN 0149-5992
WRAP_Mcternan_P_McTernan_Diabetes_Care_proof_copy_only.pdf - Accepted Version - Requires a PDF viewer such as GSview, Xpdf or Adobe Acrobat Reader
Official URL: http://dx.doi.org/10.2337/dc11-1593
OBJECTIVE-To evaluate the changes in circulating endotoxin after a high-saturated fat meal to determine whether these effects depend on metabolic disease state.
RESEARCH DESIGN AND METHODS-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.
RESULTS-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%up arrow) than NOC subjects (P < 0.05).
CONCLUSIONS-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.
|Item Type:||Journal Article|
|Subjects:||R Medicine > RC Internal medicine|
|Divisions:||Faculty of Medicine > Warwick Medical School > Translational & Systems Medicine > Metabolic and Vascular Health
Faculty of Medicine > Warwick Medical School
|Library of Congress Subject Headings (LCSH):||Non-insulin-dependent diabetes -- Nutritional aspects, Endotoxins|
|Journal or Publication Title:||Diabetes Care|
|Publisher:||American Diabetes Association|
|Number of Pages:||8|
|Page Range:||pp. 375-382|
|Access rights to Published version:||Restricted or Subscription Access|
|Funder:||British Medical Institute (BMI), Birmingham Science City, British Heart Foundation|
1. Laaksonen DE, Niskanen L, Nyyssönen K,
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