Key result
A test meal significantly reduced peak reactive hyperaemia from 52.3 to 36.8 ml min-1 100 ml-1 (P<0.005) in insulin-treated type-2 diabetics, whereas it remained unaltered in controls.
Why the study?
Does a test meal (postprandial state) impair resistance vessel reactivity in insulin-treated type-2 diabetic patients compared to fasting state and controls?
Observational (n=32)
Does a test meal (postprandial state) impair resistance vessel reactivity in insulin-treated type-2 diabetic patients compared to fasting state and controls?
Absolute Event Rate: 36.8% vs 52.3%
p-value: p=<0.005
Postprandial hyperglycaemia acutely impairs resistance vessel reactivity in insulin-treated type-2 diabetic patients, highlighting a potential mechanism for vascular dysfunction.
Postprandial reduction in reactive hyperaemia may occur in insulin-treated type-2 diabetes; hypothesis-generating and requires prospective confirmation before clinical consideration.
Reduced postischaemic reactive hyperaemia, is considered a marker of impaired resistance vessel function. Acute postprandial hyperlipidaemia has been shown to induce vascular dysfunction. In the present study, the impact of postprandial hyperglycaemia on resistance vessel reactivity was investigated in insulin treated type-2 diabetic patients. The study was performed in 16 insulin treated type-2 diabetics (eight male/eight female, age 47 +/- 3 years, HbA1c 7.2 +/- 0.2) and 16 controls. Reactive hyperaemia was measured in the forearm by venous occlusion plethysmography after 5 min of ischaemia in the fasting state and 90 min after a test meal. In diabetics, blood glucose increased from 8.7 +/- 1.1 to 15.3 +/- 1.0 mmol l-1 (P<0.001) postprandially. This resulted in (i) a significant increase of resting blood flow (3.4 +/- 0.3 to 4.8 +/- 0.4 ml min-1 100 ml-1, P<0.01) and (ii) in a reduced peak reactive hyperaemia (52.3 +/- 7.4 to 36.8 +/- 4.3 ml min-1 100 ml-1, P<0.005). In controls, a similar effect of the meal on resting flow was observed but reactive hyperaemia was unaltered. In the absence of a test meal, basal flow as well as peak reactive hyperaemia remained unchanged in diabetic as well as in non-diabetic subjects. Our data provide evidence that in the postprandial state resistance vessel reactivity becomes reduced in insulin treated type-2 diabetic patients.
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Francesconi et al. (2001) conducted an observational in Insulin treated type-2 diabetes mellitus (n=32). Test meal (postprandial state) vs. Fasting state was evaluated on Peak reactive hyperaemia (p=<0.005). A test meal significantly reduced peak reactive hyperaemia from 52.3 to 36.8 ml min-1 100 ml-1 (P<0.005) in insulin-treated type-2 diabetics, whereas it remained unaltered in controls.
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