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Transplantation. 2019 Jan;103(1):191-201. doi: 10.1097/TP.0000000000002424.

Obesity and Metabolic Syndrome in Kidney Transplantation: The Role of Dietary Fructose and Systemic Endotoxemia.

Author information

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.
4
Division 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.

Abstract

BACKGROUND:

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.

METHODS:

This cross-sectional observational study enrolled 128 KTRs longer than 1 year posttransplantation. Clinical, biochemical, anthropometric, and questionnaire assessments were undertaken.

RESULTS:

Obesity (body mass index, ≥30 kg/m) 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).

CONCLUSIONS:

Dietary modifications through decreasing fructose intake and addressing systemic endotoxemia are plausible targets for improving metabolic health of KTRs.

PMID:
30130326
DOI:
10.1097/TP.0000000000002424
[Indexed for MEDLINE]

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