PMID- 15667583
OWN - NLM
STAT- MEDLINE
DCOM- 20050503
LR  - 20111117
IS  - 0014-2972 (Print)
IS  - 0014-2972 (Linking)
VI  - 35
IP  - 2
DP  - 2005 Feb
TI  - Is postprandial hypertriglyceridaemia in relatives of type 2 diabetic subjects a 
      consequence of insulin resistance?
PG  - 117-25
AB  - BACKGROUND: Higher postprandial triglyceride responses reported in first degree 
      relatives of people with type 2 diabetes (REL) were postulated to be the result 
      of an early, possibly intrinsic, defect in oral lipid handling. The postprandial 
      triglyceride response to high fat meals (HFM) in normal subjects is reduced by 
      the insulin response to dietary carbohydrate (CHO) in the meal. The aims of this 
      study were to examine whether (1) insulin resistance is associated with an 
      intrinsic defect in triglyceride handling in insulin-resistant REL and (2) 
      insulin resistance is associated with altered triglyceride handling after HFM 
      with high CHO content. MATERIALS AND METHODS: Postprandial responses to a HFM in 
      normolipidaemic, normoglycaemic REL were compared with subjects without a family 
      history of diabetes mellitus (CON). Over 6 h, the insulin, glucose, triglyceride 
      and nonesterified fatty acid (NEFA) responses after a high fat (80 g fat), low 
      CHO (HFM-LC; 20 g CHO, 4250 kJ) meal and a high fat, high CHO (HFM-HC; 100 g CHO, 
      5450 kJ) meal were examined. RESULTS: The 10 (7F/3M) REL were significantly more 
      insulin-resistant, determined by glucose infusion during a hyperinsulinaemic 
      euglycaemic clamp than the 10 (5F/5M) CON (glucose infusion rate 44.6 +/- 4.9 vs. 
      60.0 +/- 4.8 micromol min(-1) kg FFM(-1), P = 0.037). Subjects were similar for 
      age and body mass index (BMI). The triglyceride increments after the HFM-LC were 
      similar in both, peaking at 180-240 min (Delta0.77 +/- 0.11 mmol L(-1)), 
      demonstrating no postprandial defect in REL, despite insulin resistance. There 
      was a significantly lower postprandial triglyceride response in CON following the 
      HFM-HC compared with the HFM-LC, but not in REL. In contrast, the higher insulin 
      level during the HFM-HC was associated with significantly greater NEFA level 
      suppression than in the HFM-LC (2.13 +/- 0.51 vs. 0.70 +/- 0.35 mmol L(-1), P = 
      0.03), only in the REL. CONCLUSIONS: These results are inconsistent with a 
      primary aetiological role for postprandial hypertriglyceridaemia in already 
      insulin resistant type 2 diabetic REL, but raise the possibility that this 
      potentially atherogenic manifestation is secondary to insulin resistance 
      lessening VLDL production and/or release from the liver.
FAU - Kriketos, A
AU  - Kriketos A
AD  - Diabetes and Obesity Research Program, Garvan Institute of Medical Research, 384 
      Victoria Street, Sydney, NSW 2010, Australia.
FAU - Milner, K-L
AU  - Milner KL
FAU - Denyer, G
AU  - Denyer G
FAU - Campbell, L
AU  - Campbell L
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Eur J Clin Invest
JT  - European journal of clinical investigation
JID - 0245331
RN  - 0 (Blood Glucose)
RN  - 0 (Fatty Acids, Nonesterified)
RN  - 0 (Insulin)
RN  - 0 (Lipids)
SB  - IM
MH  - Adult
MH  - Blood Glucose/metabolism
MH  - Diabetes Mellitus, Type 2/*blood
MH  - Energy Metabolism
MH  - Fatty Acids, Nonesterified/blood
MH  - Female
MH  - Glucose Clamp Technique
MH  - Humans
MH  - Hypertriglyceridemia/blood/*etiology
MH  - Insulin/blood
MH  - Insulin Resistance
MH  - Lipids/*blood
MH  - Male
MH  - Middle Aged
MH  - Obesity/blood
MH  - Postprandial Period/physiology
EDAT- 2005/01/26 09:00
MHDA- 2005/05/04 09:00
CRDT- 2005/01/26 09:00
PHST- 2005/01/26 09:00 [pubmed]
PHST- 2005/05/04 09:00 [medline]
PHST- 2005/01/26 09:00 [entrez]
AID - ECI1458 [pii]
AID - 10.1111/j.1365-2362.2005.01458.x [doi]
PST - ppublish
SO  - Eur J Clin Invest. 2005 Feb;35(2):117-25. doi: 10.1111/j.1365-2362.2005.01458.x.