Type 2 diabetes mellitus (T2DM) is a chronic disorder determined by lifestyle and genes. It is associated with chronic hyperglycaemia along with other metabolic abnormalities. It is also one of the risk factors for cardiovascular disease (CVD). This disease is due to insulin resistance and/or deficiency as well as increased hepatic glucose output. According to the Third National Health and Morbidity Survey (3rd NHMS), the prevalence of T2DM for adults aged 30 years and above is 14.9%, increased by almost 80% from 1996 to 2006. Dietary composition may affect insulin sensitivity, postprandial triacylglycerol concentration and the risk of T2DM. The role of dietary fats in T2DM is of particular interest and has been clinically studied for many decades. The type of fat we ingest every day consists of different types of fatty acids and different degree of saturation, which in turn influence glucose metabolism by altering cell membrane function, enzyme activity, insulin signalling and gene expression. Previous studies demonstrated that interesterification of dietary fat alter postprandial lipaemia. Saturated fat such as palm olein has been reported to display lower postprandial lipaemia after interesterification. Changing the structure of triacylglycerol (TAG) alters the physical properties of dietary fat which affects digestibility, metabolism and atherogenicity. A recent study conducted by Sanders and co-workers demonstrated reduced levels of plasma glucose-dependent insulinotropic polypeptide (GIP) following both the lard and interesterified palm olein (IPO) compared with the palm olein (PO) and high oleic sunflower oil (HOS) diets in healthy subjects. The GIP and glucagon-like peptide-1 (GLP-1) are major players in the modulation of postprandial insulin secretion by the pancreas. Although GIP secretion in response to meals is normal in patients with Type 2 diabetes mellitus (T2DM), GIP induced secretion of insulin is defective in diabetes. This is observed to be predominantly a defective stimulation of the late phase of insulin response (20-120 minutes). The effect of IPO on GIP may be exaggerated in T2DM patients with impaired insulin sensitivity. Hence, IPO may change the concentrations of gut hormones, postprandial lipaemia, insulinaemic response and CVD related haemostatic markers.
Subjects aged between 30 and 60 years old (male and female) with Type 2 diabetes mellitus (T2DM) will be recruited for this study. A randomized, crossover, double-blind study design will be carried out to investigate the acute effects of high fat meals prepared using palm olein (PO), chemically interesterified palm olein (IPO) and high oleic sunflower oil (HOS) (control) on study subjects with T2DM. Study subjects will have to undergo three postprandial challenges, separated by at least one week interval. Fasting blood sample and duplicate baseline blood samples will be taken in the morning of postprandial day. After that, subjects will be asked to consume a test meal consisting a high fat muffin baked using the aforementioned oils and a milkshake within 10 minutes. After meal, venous blood samples will be taken at time-points 15, 30, 60, 90, 120 min, 3 h, 4 h, 5 h, 6 h and post-heparin plasma 5 min and 15 min for analysis. Pulse wave analysis will be conducted to evaluate central blood pressure and arterial stiffness. Meal appreciation will be assessed by utilising visual analogue scale (VAS) before eating, after eating and at each time-point.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
PREVENTION
Masking
DOUBLE
Enrollment
23
Test meal consists of a high fat muffin (containing 50 g native palm olein) and a cup of milkshake, to be taken as breakfast for each postprandial study day.
Test meal consists of a high fat muffin (containing 50 g chemically interesterified palm olein) and a cup of milkshake, to be taken as breakfast for each postprandial study day.
Test meal consists of a high fat muffin (containing 50 g high oleic sunflower oil) and a cup of milkshake, to be taken as breakfast for each postprandial study day.
Malaysian Palm Oil Board (MPOB)
Kajang, Selangor, Malaysia
Hulu Langat District Health Office
Kajang, Selangor, Malaysia
Sepang District Health Office
Sepang, Selangor, Malaysia
Universiti Putra Malaysia
Serdang, Selangor, Malaysia
Selangor State Health Office
Shah Alam, Selangor, Malaysia
6-hour postprandial changes from fasting in glucose-dependent insulinotropic polypeptide (GIP)
To determine the postprandial changes of GIP.
Time frame: 0, 15, 30, 60, 90, 120 min, 3, 4, 5, 6 hour
6-hour postprandial changes from fasting in gut hormones
To determine the postprandial changes of ghrelin, glucagon-like peptide-1 (GLP-1), peptide YY (PYY) and cholecystokinin (CCK).
Time frame: 0, 15, 30, 60, 90, 120 min, 3, 4, 5, 6 h
6-hour postprandial changes from fasting in insulinaemic response
To determine the postprandial changes of glucose, insulin, C-peptide and non-esterified fatty acid (NEFA)
Time frame: 0, 15, 30, 60, 90, 120 min, 3, 4, 5, 6 hour
6-hour postprandial changes from fasting in lipaemia
To determine the postprandial changes of triacylglycerol (TAG) and apolipoprotein B48 (apoB48). To compare lipoprotein lipase (LPL) activity, chylomicron fatty acid composition and plasma fatty acid (PFA) composition across meals.
Time frame: 0, 1, 2, 3, 4, 5, 6 hour for TAG and apoB48; 6 hour postheparin for LPL; pooled 3, 4, 5 hour for chylomicron and PFA
6-hour postprandial changes from fasting in haemostatic response
To determine the postprandial changes of factor FVII activation (FVIIa), plasminogen activator inhibitor-1 (PAI-1)and D-dimer. To compare pulse wave analysis (PWA) across meals.
Time frame: 0, 2, 4, 6 hour for FVIIa, PAI-1 and D-dimer; 0, 4 hour for PWA
6-hour changes from fasting hunger rating using visual analogue scale (VAS)
To determine the changes in hunger rating and food satiety
Time frame: 0, 15, 30, 60, 90, 120 min, 3, 4, 5, 6 hour
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