(PTFS04-01-23) Increased Serum Lipopolysaccharide After a Short-Term High Fat Diet in Older Individuals With Obesity Compared to Those With Normal Body Weight: A Randomized Crossover Study

Objectives: Lipopolysaccharides (LPS), also known as endotoxins, are present in gram-negative bacteria and increased serum concentrations are associated with inflammation and a high fat diet (HFD). Additionally, individuals with obesity may have greater intestinal concentrations of gram-negative bacteria that contribute to low-grade systemic inflammation. The objective of this study was to determine whether short-term higher and lower fat intakes affect serum LPS concentration in lean and obese older individuals.

Methods: In this crossover study, obese and lean older adults (50-79 years old) were randomly assigned to first 5 days of HFD (40%) or 5 days of low fat diet (LFD; 20%) followed by the other diet. These diets were separated by a 2-week washout period. Intake during each diet was recorded by participants using food records. A 5-hour mixed meal tolerance test (performed after the LFD) included a meal with 530 calories (27g; 46% fat). Recombinant Factor C assay was used to measure serum LPS (Lonza) and lipopolysaccharide binding protein (LBP) was measured by ELISA (Invitrogen Corp.). The effect of diet on LPS and LBP was assessed using paired T-tests. Two-way repeated measures ANOVA was used to assess responses to the mixed meal in lean and obese groups (SPSS v28).

Results: Participants were 64±6 years and 66% were female. Body mass index was 24.3±1.8 kg/m² and 36.6±6.0 kg/m² in lean (n=16) and obese (n=16) individuals, respectively. Reported fat intake during the LFD was 26±6% (7±2% SFA) and 46±6% (16±3% SFA) during the HFD (p < 0.001) and did not differ between groups. Fasting serum LPS was higher after the HFD than LFD in the obese group [HF: 0.64±0.46 EU/mL vs LF: 0.36±0.20 EU/mL, p< 0.05], but not the lean group [HF: 0.42±0.35 EU/mL vs LF: 0.34±0.22 EU/mL]. The rise in postprandial serum LPS was higher in obese than lean individuals (p < 0.05). Fasting LBP concentration did not differ between HFD and LFD, and postprandial LBP concentrations were not significantly different in obese and lean groups.

Conclusions: Individuals with obesity are more susceptible to an increase in LPS due to short-term high fat intake. Furthermore, postprandial LPS showed a marked increase only in individuals with obesity that remained elevated after 5 hours. These findings may have implications for dietary fat induced inflammation in obese populations.

Funding Sources: Busch Biomedical Rutgers; USDA NIFA