title: Postprandial metabolic response to a fat- and carbohydrate-rich meal in patients with chronic kidney disease.
abstract: BACKGROUND
  While chronic kidney disease (CKD) is associated with dysmetabolism including a marked insulin resistance, the postprandial response has not comprehensively been studied in CKD patients.
  
  
  METHODS
  We conducted an intervention study comparing fasting and postprandial circulating biomarkers of glucose and lipid homeostasis, incretins, anabolic hormones, inflammation and oxidative stress in nine prevalent non-diabetic hemodialysis (HD) patients and 10 matched controls assessed after a standardized meal consisting of 75 g of milk fat, 80 g of carbohydrates and 6 g of proteins/m(2) of body surface area.
  
  
  RESULTS
  Glucose and triglyceride increased in a similar manner following the meal, while insulin, C-peptide and glucose-dependent insulinotropic polypeptide increased more in HD patients. HDL and LDL cholesterol decreased slightly with no significant difference between the groups. The elevated baseline growth hormone (GH) in patients dropped, resulting in comparable levels in both groups 240 min after the meal; however, there was no change in insulin-like growth factor 1 (IGF-1) levels. No marked changes of interleukin 6 and tumor necrosis factor-α were observed in either group. An elevation in the DNA oxidative product 8-hydroxydeoxyguanosine was observed in HD patients.
  
  
  CONCLUSIONS
  The postprandial state in CKD is characterized by impaired insulin sensitivity with increased incretin levels, along with GH/IGF-1 axis uncoupling and an elevation in an oxidative stress marker.
authors.affiliation: Division of Renal Medicine and Baxter Novum, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden.
authors.forename: Tetsu
authors.initials: T
authors.lastname: Miyamoto
authors.forename: Abdul
authors.initials: A
authors.lastname: Rashid Qureshi
authors.forename: Tae
authors.initials: T
authors.lastname: Yamamoto
authors.forename: Ayumu
authors.initials: A
authors.lastname: Nakashima
authors.forename: Bengt
authors.initials: B
authors.lastname: Lindholm
authors.forename: Peter
authors.initials: P
authors.lastname: Stenvinkel
authors.forename: Anders
authors.initials: A
authors.lastname: Alvestrand
authors.forename: Jonas
authors.initials: J
authors.lastname: Axelsson
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D001786:Blood Glucose / Q000378:metabolism; D016022:Case-Control Studies; D003404:Creatinine / Q000378:metabolism; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000378:metabolism; D004040:Dietary Carbohydrates / Q000494:pharmacology*; D004041:Dietary Fats / Q000494:pharmacology*; D005215:Fasting; D005260:Female; D005500:Follow-Up Studies; D005919:Glomerular Filtration Rate; D013006:Growth Hormone / Q000097:blood; D006801:Humans; D007328:Insulin / Q000378:metabolism; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D007676:Kidney Failure, Chronic / Q000378:metabolism*; D007677:Kidney Function Tests; D008297:Male; D008875:Middle Aged; D019518:Postprandial Period / Q000502:physiology*; D011379:Prognosis; D014280:Triglycerides / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D004040:Dietary Carbohydrates; D004041:Dietary Fats; D007328:Insulin; D015850:Interleukin-6; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D007334:Insulin-Like Growth Factor I; D000080242:8-Hydroxy-2'-Deoxyguanosine; D013006:Growth Hormone; D003404:Creatinine; D003849:Deoxyguanosine