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- Olive (Olea europaea, Oleaceae) Oil
- Postprandial Glycemic Response
- Type 1 Diabetes
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Date:
09-15-2016 | HC# 031633-552
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Re: Olive Oil Reduces Postprandial Glycemic Response in Patients with Type 1 Diabetes
Bozzetto
L, Alderisio A, Giorgini M, et al. Extra-virgin olive oil reduces glycemic
response to a high-glycemic index meal in patients with type 1 diabetes: a
randomized controlled trial. Diabetes
Care. April 2016;39(4):518-524.
Postprandial
glycemic response is an important factor in controlling blood glucose in
persons with type 1 diabetes. Although carbohydrate content of a meal is
considered the main dietary factor influencing postprandial glycemia, growing
evidence suggests the fat content of a meal also influences glycemic response.
These authors conducted a randomized, crossover study in patients with type 1
diabetes to test the hypothesis that monounsaturated fat from extra virgin
olive (Olea europaea, Oleaceae)
oil (EVOO) would reduce postprandial glycemic response.
Thirteen
patients with type 1 diabetes (8 women and 5 men) were recruited from the
diabetes care unit of the Federico II University teaching hospital in Naples,
Italy. Inclusion criteria included treatment with continuous subcutaneous
insulin infusion, the use of fast-acting insulin analogs for at least 6 months,
and a glycated hemoglobin (HbA1c) <8.0%. The mean age of the patients was 38
± 11 years; body mass index was 24.8 ± 2.9 kg/m2. Duration of
diabetes was 25 ± 3 years. The total daily insulin dose among the patients was
41.1 ± 10.7 IU; they had acceptable blood glucose levels.
Before
the start of the study, the patients took part in a 1-week run-in period during
which they underwent continuous glucose monitoring (CGM) and completed a 7-day
dietary record to optimize basal infusion rate and insulin-to-glycemic load
ratio. The patients were randomly assigned to a 1-week period during which they
consumed either 3 high-glycemic index (HGI) meals or low-glycemic index (LGI)
meals. They then crossed over to the alternative meals for 1 week. The HGI and
LGI meals were similar in total carbohydrate content but differed in amount and
type of fat and were categorized as low in fat (low-fat), high in saturated fat
(butter), or high in monounsaturated fats from EVOO. During the 2 weeks of the
study, the patients wore sensors at all times for CGM. The patients checked
capillary blood glucose at 2, 4, and 6 hours after the test meals.
The study procedures were the same for both test weeks. The 3 test meals were
eaten at lunch on days chosen according
to the patients' work and recreational activities to keep these activities
reproducible and compatible with the study design. On the mornings of the test
meal days, the patients ate the same light breakfast to avoid a second-meal
effect bias. They avoided strenuous physical activity on the day before the
test meal, the morning of the test meal, and for 6 hours after the meal. Pre-meal
insulin doses, which were based on the insulin-to-glycemic load ratio
determined for each patient, were significantly lower before the LGI meals
compared with doses administered before the HGI meals (P < 0.0001).
The
EVOO and butter meals were similar in energy content; the low-fat meal had a
lower energy content. The glycemic index was about 25% greater in the HGI meals
than in the LGI meals. Dietary fiber was greater (by about 13 g) in the LGI meals
compared with the HGI meals.
The
HGI meals included white rice (Oryza sativa,
Poaceae) (60 g), white bread (75 g), minced beef (90 g), and banana (Musa paradisiaca, Musaceae) (180 g),
plus butter (43 g) or EVOO (37 g). The LGI meals included pasta (50 g), lentils
(Lens culinaris, Fabaceae) (100 g),
whole-meal bread (30 g), ham (15 g), and apple (Malus pumila, Rosaceae) (185 g), plus butter (45 g) or EVOO (37 g).
The
authors report that the 6-hour postprandial glucose profile was significantly
different between HGI and LGI meals (P=0.005), being significantly higher
during the first 3 hours after the HGI meals with a tendency to an opposite
pattern later. Although the time to glucose peak was significantly delayed
after LGI compared with HGI meals (P=0.003), no significant differences were
observed in the peak values between the LGI (4.7 ± 0.7 mmol/L) and HGI (5.3 ±
0.9 mmol/L) meals. The quality and amount of fat in the LGI meals did not
significantly influence postprandial blood glucose response, blood glucose
peak, or time to glucose peak.
With
the HGI meals, postprandial blood glucose was significantly lower after EVOO
than after low-fat or butter meals (P<0.0001), with a marked difference from
baseline to 3 hours between EVOO and either low-fat or butter (P<0.05) meals.
The blood glucose peak was lower, although not significantly, after the EVOO
meal than after the butter or low-fat meals. The time to blood glucose peak was
significantly delayed after the EVOO meal (190 ± 101 minutes) compared to after
the butter (188 ± 104 minutes) or low-fat (146 ± 81 minutes) meal (P=0.035).
In
this study, the type of fat significantly influenced the postprandial glycemic
response in patients with type 1 diabetes. The addition of different types of
fats to meals with an LGI did not influence postprandial blood glucose
response; however, different types of fats added to HGI meals did influence the
response. These results, which indicate that the combination of carbohydrate
foods and type of fat should be considered when determining the timing and dose
of prandial insulin administration, have important clinical implications for
persons with type 1 diabetes. A possible weakness of this study is the
consumption of meals at the patient's home without direct supervision, which
could have affected the standardization of procedures. The home setting also
limited the gathering of information on possible mechanisms responsible for the
results.
—Shari Henson
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