Background: Abdominal obesity and exaggerated postprandial lipemia are independent risk factors for cardiovascular disease (CVD) and mortality, and both are affected by dietary behavior.
Objective: We investigated whether dietary supplementation with whey protein and medium-chain saturated fatty acids (MC-SFAs) improved the postprandial lipid metabolism in humans with abdominal obesity.
Design: We conducted a 12-wk, randomized, double-blinded, diet intervention study. Sixty-three adults were randomly allocated to one of 4 diets in a 2 × 2 factorial design. Participants consumed 60 g milk protein (whey or casein) and 63 g milk fat (with high or low MC-SFA content) daily. Before and after the intervention, a high-fat meal test was performed. We measured changes from baseline in fasting and postprandial triacylglycerol, apolipoprotein B-48 (apoB-48; reflecting chylomicrons of intestinal origin), free fatty acids (FFAs), insulin, glucose, glucagon, glucagon-like peptide 1 (GLP-1), and gastric inhibitory polypeptide (GIP). Furthermore, changes in the expression of adipose tissue genes involved in lipid metabolism were investigated. Two-factor ANOVA was used to examine the difference between protein types and fatty acid compositions, as well as any interaction between the two.
Results: Fifty-two participants completed the study. We found that the postprandial apoB-48 response decreased significantly after whey compared with casein (P = 0.025) independently of fatty acid composition. Furthermore, supplementation with casein resulted in a significant increase in the postprandial GLP-1 response compared with whey (P = 0.003). We found no difference in postprandial triacylglycerol, FFA, insulin, glucose, glucagon, or GIP related to protein type or MC-SFA content. We observed no interaction between milk protein and milk fat on postprandial lipemia.
Conclusion: We found that a whey protein supplement decreased the postprandial chylomicron response compared with casein in persons with abdominal obesity, thereby indicating a beneficial impact on CVD risk.
Alex’s Notes: Milk is undoubtedly an omnipresent food in the human diet. It is the first food of mammals and research supports a strong constant association of milk consumption and health. The nutritional richness of milk is unquestionable; it is a good source of high-quality proteins with multiple roles in immune function, as well as nutrient transport and absorption. We have previously seen that one of the proteins within dairy – whey protein – has the ability to regulate appetite, promote favorable changes in body composition, and modify skeletal muscle gene expression.
However, it is also interesting to note the associations between dairy fat and health, such as improved glucose tolerance and insulin sensitivity. Dairy fat is primarily saturated, but contains a solid 10% as medium-chained triglycerides (MCTs), which bypass nearly the entire long-chained fatty acid (LCFA) absorption process. MCTs are transported directly to the liver, whereas LCFAs must first be incorporated into chylomicrons with the apolipoprotein (Apo) B-48. These chylomicrons then travel throughout the bloodstream to deliver their fatty payload to the body before returning to the liver as chylomicron remnants. Unfortunately, these remnants take part in the formation of atherosclerotic plaques.
So what does this leave us with? Well, it is completely possible that the benefits associated to dairy fat were actually just an effect of the protein content, but that wouldn’t explain why some associations are not seen in low-fat dairy. MCTs are truly limited in nature, existing only in a few food products. Dairy is one, and coconut is probably the most well-known. Thus, these types of fats are really the only thing unique about dairy fat, and thus could be the answer we are looking for.
The aim of the present study was primarily to investigate the long-term effects of whey and MCT supplementation on postprandial concentrations of apoB-48, triglyceride, and free fatty acids (FFAs) and on the expression of genes involved in the lipid metabolism in the subcutaneous adipose tissue.
Setting things up
This study was the gold-standard: a randomized, parallel-controlled, double-blinded, 12-week intervention. Fifty-two participants with abdominal obesity but not type-2 diabetes, cardiovascular, renal, endocrine, or psychiatric diseases completed the study. They were divided into four groups:
- Whey + low-dose MCT (WL)
- Whey + high-dose MCT (WH)
- Casein + low-dose MCT (CL)
- Casein + high-dose MCT (CH)
Each and every day during the 12-week intervention, the participants had to consume 60 grams of their trial protein (whey or casein) mixed in water, as well as two rolls, one cake, and 25g of butter that provided a total of 63 grams of milk fat. The total energy content of the provided dairy foods was 1480 kcal, providing 42% of kcal as fat, 21% protein, and 37% carbohydrate. All participants completed a 3-day food log prior to the intervention and had energy requirements estimated from equations, both of which a registered dietitian used to instruct the subjects on how to incorporate the test products into their regular diet while maintaining weight stability.
Before and after the intervention, and after an overnight fast, the subjects had an abdominal fat biopsy performed and had blood collected for analysis. Afterwards, they consumed a test meal consisting of bread, egg, butter, bacon, cheese, salami, milk, and decaf coffee providing 1070 kcal (65% fat, 19% carb, & 16% protein). During the following six hours, blood draws were continued.
WAIT! What about the MCTs?
Actually, this part is pretty interesting. The researchers called upon 50 Holstein cows from the Danish Cattle Research Center in Denmark to produce the two different MCT composition dairy products. For two weeks the cows were fed a low-fat diet, one that would be similar to that of nature (unless grass has fat in it), in order to increase the de novo synthesis of MCTs within the milk that was used to produce the dairy products in the high-dose MCT groups. Afterward, the cows were fed a diet supplemented with fractionated palm fat and milk was collected for the low MCT group foods.
The average daily intake of MCTs was 8.5g in the high-MCT groups and 6.9g in the low-MCT groups. Although a very minor 1.6g (24%) difference, it must be stressed that this difference reflects what could reasonably be expected to be obtained naturally.
That uncontrolled dietary intake though
Honestly, I have no idea how the researchers expected to add nearly 1500 kcal to the daily diets of abdominally obese persons and not have them increase their bodyweight. Interestingly enough, the WH, CL, and CH groups all significantly increased their bodyweight by 1.4-2 kg (3-4.4 lbs), while the WL group only tended (p=0.087) to increase their bodyweight by 1 kg (2.2 lbs). Along these lines, while all groups had an increased energy intake as a result of the intervention when compared to baseline, the casein groups consumed significantly more than the whey protein groups.
Neither fasting nor postprandial triglyceride nor FFA concentrations changed significantly in any of the groups, but whey significantly decreased the postprandial apoB-48 concentrations compared to casein, regardless of MCT status. Whether the difference in apoB-48 responses is related to changes in the chylomicron secretion or clearance remains unknown and the lower apoB-48 response to whey compared with casein may be related to differences in the uptake of triglycerides (whey protein delays the uptake). However, the reduction in postprandial apoB-48 after whey was not reflected in a change in postprandial triglycerides, suggesting that perhaps the total amount of fat in the postprandial phase is incorporated into fewer chylomicrons after whey than after the casein. The implications of this are again unknown.
Casein did have the upper-hand on whey when it came to stimulating GLP-1, which can attenuate the postprandial rise in triglycerides. Other blood-borne markers such as fasting glucose, insulin, and glucagon, and their postprandial response were unaltered in all groups.
That gene expression though
The findings in this area were very dispersed, and there was an interaction between both the fat and the protein of the groups, making it difficult to determine whether the changes could be explained by the diet intervention. For instance, gene expression of fasting LPL, GPR120, and CD36 were all upregulated in the CH group, but postprandial expression of GPR120 and CD36 were suppressed. No changes were seen in the CL group, but GPR120 and CD36 were upregulated and postprandial LPL and GPR120 down regulated in the WL group.
So the main finding is that whey significantly decreased the postprandial apoB-48 concentrations. And with this piece of the puzzle, we still have much to learn. What is the minimal and optimal dose of whey to improve postprandial apoB-48 responses? Why does whey improve the postprandial apoB-48 response but not the triglyceride response? What is the physiologic mechanism that underlies the improvement of apoB-48? Why does any of this matter?