The concepts that obesity is merely a consequence of overeating, and that metabolic health then reflects obesity, may be insufficient and potentially flawed. The role of fructose intake and metabolic endotoxemia has gained attention recently, but data in kidney transplantation are lacking. This study evaluated the risk factors for metabolic syndrome (MS), its components, and other associated markers in kidney transplant recipients (KTRs), focusing particularly on fructose intake and systemic endotoxemia.
This cross-sectional observational study enrolled 128 KTRs longer than 1 year posttransplantation. Clinical, biochemical, anthropometric, and questionnaire assessments were undertaken.
Obesity (body mass index, ≥30 kg/m2) and MS (International Diabetes Federation Definition) were found in 36.7% and 50% of KTRs, respectively. Both increased fructose intake (P = 0.01) and endotoxin level (P = 0.02) were independently associated with MS; and higher fructose intake was independently associated with obesity (P < 0.001). Specifically, increased fructose intake was associated with the central obesity (P = 0.01) and hyperglycemia (P < 0.001) criteria of MS, whereas higher endotoxin level was associated with the hypertriglyceridemia (P = 0.003) and low HDL cholesterol concentration (P = 0.002) criteria of MS. Neither saturated fat nor total caloric intakes were independently associated with obesity and MS; and neither obesity nor central obesity were independently associated with the dyslipidemia and hyperglycemia criteria of MS. Principal component analysis demonstrated relationships between higher levels of endotoxin, soluble endothelial selectin, triglycerides, and insulin resistance (r > 0.6), as well as relationships between increased fructose intake, inflammation, and blood glucose (r > 0.6).
Dietary modifications through decreasing fructose intake and addressing systemic endotoxemia are plausible targets for improving metabolic health of KTRs.
1 Department of Nephrology and Kidney Transplantation, Queen Elizabeth Hospital Birmingham, Mindelsohn Way, Edgbaston, Birmingham, United Kingdom.
2 Department of Nutrition and Dietetics, Queen Elizabeth Hospital Birmingham, Edgbaston, Birmingham, United Kingdom.
3 Division of Biomedical Statistics & Informatics, Department of Health Sciences Research, Mayo Clinic, Rochester, MN.
4Division of Transplantation Surgery, Department of Medicine, Mayo Clinic, Rochester, MN.
5 The William J. von Liebig Center for Transplantation and Clinical Regeneration, Mayo Clinic, Rochester, MN.
6 School of Infection and Immunity. University of Birmingham, Edgbaston, Birmingham, United Kingdom.
Received 21 March 2018. Revision received 3 August 2018.
Accepted 3 August 2018.
The authors declare no conflict of interest.
The research was carried out at the National Institute of Health Research (NIHR)/Wellcome Trust Clinical Research Facility based at University Hospitals Birmingham National Health Service (NHS) Foundation Trust and University of Birmingham. The views expressed are those of the authors and not necessarily those of the NHS, the NIHR, or the Department of Health.
W.C. received a research grant from the British Renal Society and was awarded a PhD research training fellowship from the National Health Service West Midlands Strategic Healthy Authority.
W.C. and R.B. designed the research. W.C., B.S., M.S., and R.B. wrote the article. W.C. and R.B. conducted the research. W.C., B.S., and R.B. analyzed the data and performed the statistical analysis. R.B. had primary responsibility for the final content.
Correspondence: Richard Borrows, MA, Department of Nephrology & Kidney Transplantation, Area 5, Level 7, Queen Elizabeth Hospital Birmingham, Mindelsohn Way, Edgbaston, Birmingham B15 2WB, United Kingdom. (Richard.Borrows@uhb.nhs.uk).
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