Bariatric surgery improves lipoprotein profile in morbidly obese patients by reducing LDL cholesterol, apoB, and SAA/PON1 ratio, increasing HDL cholesterol, but has no effect on cholesterol efflux capacity.

BACKGROUND: Bariatric surgery has been shown to reduce cardiovascular events and cause-specific mortality for coronary artery disease in obese patients. Lipoprotein biomarkers relating to low-density lipoprotein (LDL), high-density lipoprotein (HDL), their subfractions, and macrophage cholesterol efflux have all been hypothesized to be of value in cardiovascular risk assessment. OBJECTIVES: The objective of this study was to examine the effect of a lifestyle intervention followed by bariatric surgery on the lipid profile of morbidly obese patients. METHODS: Thirty-four morbidly obese patients were evaluated before and after lifestyle changes and then 1 year after bariatric surgery. They were compared with 17 lean subjects. Several lipoprotein metrics, serum amyloid A (SAA), serum paraoxonase-1 (PON1), and macrophage cholesterol efflux capacity (CEC) were assessed. RESULTS: Average weight loss after the lifestyle intervention was 10.5% and 1 year after bariatric surgery was 33.9%. The lifestyle intervention significantly decreased triglycerides (TGs; -28.7 mg/dL, P < .05), LDL cholesterol (LDL-C; -32.3 mg/dL, P < .0001), and apolipoprotein B (apoB; -62.9 µg/mL, P < .001). Bariatric surgery further reduced TGs (-36.7 mg/dL, P < .05), increased HDL cholesterol (+12 mg/dL, P < .0001), and reductions in LDL-C and apoB were sustained. Bariatric surgery reduced large, buoyant LDL (P < .0001), but had no effect on the small, dense LDL. The large HDL subfractions increased (P < .0001), but there was no effect on the smaller HDL subfractions. The ratio for SAA/PON1 was reduced after the lifestyle intervention (P < .01) and further reduced after bariatric surgery (P < .0001). Neither the lifestyle intervention nor bariatric surgery had any effect on CEC. CONCLUSIONS: Lifestyle intervention followed by bariatric surgery in 34 morbidly obese patients showed favorable effects on TGs, LDL-C, and apoB. HDL cholesterol and apoA1 was increased, apoB/apoA1 ratio as well as SAA/PON1 ratio reduced, but bariatric surgery did not influence CEC.

Soluble CD14 is associated with markers of vascular dysfunction in bariatric surgery patients.

BACKGROUND: Chronic endotoxemia has been proposed to contribute to obesity-related complications. We aimed to investigate the potential impact of lipopolysaccharide (LPS) and subsequent monocyte activation measured as soluble CD14 (sCD14) on markers of vascular dysfunction in obese subjects undergoing bariatric surgery. METHODS: This was a prospective study of 49 obese patients and 17 controls, assessed by plasma levels of LPS, sCD14, asymmetric dimethylarginine (ADMA), and symmetric dimethylarginine (SDMA). RESULTS: Levels of ADMA were increased in obese subjects compared to controls, but were not significantly reduced after bariatric surgery. In obese subjects at baseline, there was a significant trend to increasing levels of ADMA and SDMA through tertiles of sCD14 and decreasing levels of both markers through tertiles of LPS. In models adjusting for age and gender, sCD14 but not LPS remained independently associated with ADMA and SDMA. For every 10% age- and gender-adjusted increase in sCD14, ADMA increased 0.031 µM (5.6%), whereas SDMA increased 0.039 µM (10.8%). CONCLUSIONS: Our results suggest that monocyte activation as measured by sCD14 is associated with obesity-related vascular dysfunction, whereas potential upstream triggers including microbial products should be investigated in future studies.

Plasma lipopolysaccharide is closely associated with glycemic control and abdominal obesity: evidence from bariatric surgery.

OBJECTIVE: It is of vital importance to elucidate the triggering factors of obesity and type 2 diabetes to improve patient care. Bariatric surgery has been shown to prevent and even cure diabetes, but the mechanism is unknown. Elevated levels of lipopolysaccharide (LPS) predict incident diabetes, but the sources of LPS are not clarified. The objective of the current study was to evaluate the potential impact of plasma LPS on abdominal obesity and glycemic control in subjects undergoing bariatric surgery. RESEARCH DESIGN AND METHODS: This was a prospective observational study involving a consecutive sample of 49 obese subjects undergoing bariatric surgery and 17 controls. Main assessments were plasma LPS, HbA1c, adipose tissue volumes (computed tomography), and quantified bacterial DNA in adipose tissue compartments. RESULTS: Plasma levels of LPS were elevated in obese individuals compared with controls (P < 0.001) and were reduced after bariatric surgery (P = 0.010). LPS levels were closely correlated with HbA1c (r = 0.56; P = 0.001) and intra-abdominal fat volumes (r = 0.61; P < 0.001), but only moderately correlated with subcutaneous fat volumes (r = 0.33; P = 0.038). Moreover, there was a decreasing gradient (twofold) in bacterial DNA levels going from mesenteric via omental to subcutaneous adipose tissue compartments (P = 0.041). Finally, reduced LPS levels after bariatric surgery were directly correlated with a reduction in HbA1c (r = 0.85; P < 0.001). CONCLUSIONS: Our findings support a hypothesis of translocated gut bacteria as a potential trigger of obesity and diabetes, and suggest that the antidiabetic effects of bariatric surgery might be mechanistically linked to, and even the result of, a reduction in plasma levels of LPS.