Chicken, Rice, Veggies & Oil and How Their Effects on Your Insulin & Glucose Levels Are 50% Off Those You'd Expect Based on the Calculated Glycemic Index of This Meal

The power of GI calculations is limited and even with meals as simple as the one in the picture, the calculated glycemic index can be ~50% off!

As a SuppVersity reader you've repeatedly read about macronutrient interactions, such as the insulin boosting effects of whey protein or dietary fat, studies that investigate the effects of the individual ingredients of a complete meal on the glycemic response healthy men and women, however, are scarce. Against that background the results of a recent study from the Clinical Nutrition Research Centre at the Singapore Institute for Clinical Sciences are of particular interest. After all, the Lijun Sun et al. (2014) determined the effect of co-ingesting a high-protein food (breast chicken), a fat (ground nut oil), a leafy vegetable or all three on the glycaemic and insulinaemic responses of white rice in healthy adults and did thus produce results that could be practically relevant for all of us - more relevant than inaccurately calculated GIs.

Use sugar alternatives if you want to improve your blood glucose!

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Artif. Sweetened Foods Good, Not Bad for Fat Loss.

Before we get to the study results, though, let's briefly recap what the researchers actually did: Sun et al. recruited twelve healthy participants (six female and six male) by means of advertisements, flyers and personal communications.

"Before inclusion into the study, potential participants were briefed on all aspects of the experiment and were given the opportunity to ask questions. Following the securing of consent, a health assessment was performed which included anthropometric measurements and a health questionnaire (giving details of food allergies/intolerance, metabolic diseases, special dietary needs and smoking habits). Those who fulfilled all the inclusion criteria [body mass index 18.5–24.99 kg/m2; blood pressure (BP)—systolic BP between 110 and 120 mmHg and diastolic BP between 75 and 85 mmHg; age 21–50 years; fasting blood glucose, 4–6 mmol/L; not on prescription medication, non-smoking; no genetic or metabolic diseases) were enrolled into the study." (Sun. 2014)

In addition, the amount of regular physical activity was quantified and subjects who were partaking in competitive sports and endurance events were excluded. Eventually, the scientists ended up with a group of normal-weight men and women at the age of 21–34 years.

Table 1: Composition of the test meals, ACHO = available carbohydrates.
Nutritional data were obtained from the manufacturers (Sun. 2014).

The subjects visited the laboratory 5 times (plus a baseline testing with a glucose solution). On each of these testing sessions, which were separated by at least one week, the subjects arrived at the laboratory between 7:30 and 8:30 after an overnight fast and received one of the five test meals from Table 1, which contained 194 g white of plain white rice,  254 g of white rice with fat, 294 g of plain white rice with chicken breast, 314g of white rice with vegetable and 474g of white rice with fat, chicken and vegetable, respectively.

Ground nut oil? I guess most of you will know the oil that was used in the study at hand as "peanut oil" and it is - as you will probably know, as well - not exactly high in "holy" omega-3 fatty acids. Rather than that, peanut oil contains oleic acid (46.8% as olein), linoleic acid (33.4% as linolein), and palmitic acid (10.0% as palmitin), as well as small amounts of stearic acid, arachidic acid, arachidonic acid, behenic acid, lignoceric acid, but not a singly milligram of omega-3s.
The test or reference food was then given to consume within 15 min. Further blood samples for glucose and insulin analysis were taken for the subsequent 180 min (every 15 min in the first hour and every 30 min for the subsequent hours) - a procedure that yielded the following results.

Figure 1: Glucose levels expressed relative to the ingestion of 250g of glucose (Sun. 2014)

The values in Figure 1 are expressed relative to the glucose response to 250g of pure glucose, of which a brief glimpse at the data tells you that they produce higher peak and incremental area under the curve (iAUC, a measure for the glycemia over the whole testing period) levels than any of the meals. Statistical significant differences were yet observed only for rice with chicken breast, rice with vegetable, and rice with fat, chicken and vegetable - yet not for the plain rice and the rice + fat meal (the latter was to be expected based on the discussion in my previously referenced article "True or False? Adding Fat to A Carby Meal Lowers Insulin Response" | read more).

Significant differences for the insulin response were observed for the white rice + chicken meal, where the insulin response was significantly higher compared to the white rice only (+22%), as well as the rice with + vegetable meal, where the insulin response was significantly lower compared to the white rice only condition (-16%).

The combination of foods determines the GI of the meal

Based on the classic equation that's usually used to determine the glycemic index of a meal (Hätönen. 2011), Sun et al. calculated the predicted glycemic of the five test meals and compared it to the actual glycemic index (GI) that was calculated based on the measured glucose and insulin response of the subjects.

Figure 2: Predicted and measured glycemic index as well as measured insulinemic index of the meals (Sun. 2014)

As you can see in Figure 2, the comparison yields an unsurprising result. As it's usually the case, when simple equations are used to predict physiological effects, the real GI values were significantly different from the calculated ones and  - significantly lower, that is. Accordingly, the meal with the least impact on postprandial glycemia and a comparatively low insulinemic effect is the one containing rice, fat, chicken and veggies - in other words, the complete meal. 

Suggested Read: "Get Your Protein, Veggies & Fruits and Get Them Regularly: High(er) Meal Frequency (6 à Day) + High(er) Protein Diet Support Weight & Fat Loss on a Diet." | read more

Bottom line: While the importance of the glycemic index (GI) has long been totally overrated, there is accumulating evidence that high postprandial glucose levels are a significant contributor to increases in cardiovascular disease risk even in healthy individuals (Einarson. 2011; Mah. 2011). Against that background the results of this recent trial support my previous recommendation to consume balanced meals containing protein, fat and carbohydrates, instead of no-fat or no-carb meals.

In contrast to what the "paleo hypothesis" and the notion that our ancestors would not have collected some berries or boiled some rice to have it alongside the chicken they just caught would say, the contemporary scientific evidence indicates that we are well equipped to handle complex meals, as long as they don't contain exorbitant amounts of fat and carbohydrates.

One thing we should not forget, though, is that the 50% discrepancy between the calculated and real glycemic index of the "complex" test meal (four ingredients is not exactly "complex", actually) suggests that one of the reasons that many of the previous studies failed to detect a meaningful association between the (obviously calculated) GI of an individuals diet and his / her cardiovascular or diabetes risk may be that the data the scientists used was similarly inaccurate as the predicted glycemic indices of the test meal in the study at hand | Comment on Facebook!

References:

• Hätönen, Katja A., et al. "Protein and fat modify the glycaemic and insulinaemic responses to a mashed potato-based meal." British Journal of Nutrition 106.02 (2011): 248-253.
• Mah, Eunice, et al. "Postprandial hyperglycemia impairs vascular endothelial function in healthy men by inducing lipid peroxidation and increasing asymmetric dimethylarginine: arginine." The Journal of nutrition 141.11 (2011): 1961-1968. 
• Sun, Lijuan, et al. "Effect of chicken, fat and vegetable on glycaemia and insulinaemia to a white rice-based meal in healthy adults." European journal of nutrition (2014): 1-8.
• Wolever, T. M. S. "Is glycaemic index (GI) a valid measure of carbohydrate quality&quest." European journal of clinical nutrition 67.5 (2013): 522-531.

Instant Coffee, Glycemia & Caffeine Powered Post-Workout Glycogen Repletion. Fish Oil, Arachidonic Acid Release & Prostaglandin Modulation. Adipocyte Sizes & Yoyo Dieting

Judged by the way they are looking at each other they don't care about their differential glucose / insulin response too coffee, but if you do, I suggest you scroll down and read the pertaining news item.

7.3% and 21.4%, those are the SuppVersity figures of the week. Figures that stand for the 2011 youth- and 2010 adult obesity rates in Colorado and they represent the nationwide "optimum" - at least according to CDC data from the respective years. Now, it was already hard to find US states with obesity rates below the nationwide average of 13% (youths) and 27.6% (adults). What is yet even harder or rather impossible is to dig up studies which try to elucidate why Colorado is the "leanest" of the 50 US states. Non-exhausting physical activity, for example, would be a candidate, but according to Wyatt et al. the "[e]ven in Colorado, one of the leanest states, very low levels of physical activity are seen in much of the population." (Wyatt. 2005).

Wouldn't it be worth taking some time to try to elucidate what the citizens in Colorado may be doing, their fellow Americans in Mississippi (highest adult obesity rate of 34.5%) or Alabama (highest youth obesity rates of 17%) ain't doing? Are they maybe having more or less fish oil or drinking only half the amount of caffeine? I don't know, but based on today's installment of "On Short Notice", you should be able to answer whether or not it is likely that factors like these could make a difference ;-)

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Coffee, Sex and Your Physique (Gavrieli. 2013) -- The latter two, i.e. sex and your physique are what determines your postprandial glucose and insulin concentrations after escalating dosages of caffeinated coffee. That's at least what Anna Gavrieli from the Harokopio University in Athens and her colleagues from overseas write in a soon-to-be-published paper.

To examine the effects of different amounts of coffee on blood glucose and insulin concentrations in the postprandial phase (after a meal) the scientist recruited thirty-three volunteers [16♀/17♂, 16 normal-weight and 17 overweight/obese, 27.3 ± 7.2 (19–44) y] who came to the lab fasted and obviously without having  had a "wake up coffee" early in the morning. When they arrived, the subjects received a standardized meal, i.e. a slice white bread, 5 g of butter and 10 g of white sugar, providing 142 kcal (6.5% of energy from proteins, 62.5% from carbohydrates and 31.0% from lipids) along with 200 mL of water or instant coffee containing either 3 or 6 mg of caffeine/kg body weight on three different occasions.

Figure 1: Usual and experimental caffeine intake in the subjects (left); effects on glucose metabolism after standardized "breakfast" (=sugar binge) + water or different dosages of instant coffee (Gavrieli. 2013)

As you can see in figure 1, the blood samples the scientists obtained before, immediately after and in regular intervals over the remaining 3 hours after the ingestion of the "breakfast" do support the hypothesis that men and women, light and heavy weights react very differently to the ingestion of 200-500mg.

So what's the verdict then? Is coffee the way to go?

Post workout caffeine supplementation?! Just like dieting, working out is one of the confounding factors which render results like the one at hand valid only in certain scenarios. Against that background it is not surprising that a 2008 study by Pedersen et al., the results of which I have plotted for you in the figure above (Pedderson. 2013), found statistically significant improvements in glycogen resynthesis w/ 8mg/kg caffeine being coingested with 4mg/kg glucose after a workout. Whether this will yield real world benefits is obviously another story ;-)

While coffee delayed the rise of insulin in response to the standardized meal and the fall of glucose concentrations from its maximum levels in the entire study sample, the glucose incremental area under the curve (IAUC) was not just different between the interventions (with both coffee amounts inducing a greater area compared to water, p = 0.009), but also varied according to the sex and body weight of the subjects:

"Secondary, subgroup analysis at the nominal level showed that this might be more evident among females (PIAUC = .05) and overweight/obese participants (PIAUC = .03). Furthermore, coffee, mainly the 6 mg dose, could be lowering insulin concentrations the first 30 min after its consumption compared to water in men and overweight/obese participants." (Gavrieli. 2013)

So what do we make of these results, now? Well, first of all, even if your breakfast does not deserve the name food, having a single regular sized cup of coffee is unlikely to to any harm. Reversing the ratio of breakfast to coffee on the other hand and having a "Sex & The City" breakfast with a croissant and a large cup of breakfast will have you run the risk of having high blood sugar afterwards (esp. if you drink that 400mg+ pot of coffee with tons of sugar).

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The tissue incorporation of regular triglyceride based fish oils is inferior to their phospholipid bound brethren. Want to learn more? Check out my article on that matter from June 2012 (learn more)

3g of fish oil modulate the eicasonoid production from omega-6 fatty acids in young men (Zulyniak. 2013) -- 2g of EPA and 1g of DHA that was the dosage the 10 young healthy males (23.4 ± 1.7 years) had to consume on every day of the 3-months supplementation period in Zulyniak et al.'s experiment which was designed to "better understand the potential health benefits of fish oil supplementation in young healthy males" (Zulyniak. 2013).

What the researchers observed were the expected decreases in serum triglycerides (-38%), a significant increase in the proportion of HDL-c relative to total cholesterol, as well as - and this is the actual news - an increase in eicosanoids production, namely prostaglandin-F2α (P < 0.0001) and thromboxane-B2 (P = 0.0296), after fish oil supplementation.

The latter two are products of omega-6 metabolism and confirm the replacement of arachidonic acid (AA, the long-chain omega-6 fatty acid and the quasi-analogon to DHA) in the cell membranes of the erythrocytes by EPA and DHA. This process must have triggered the increase in PGF2α and TXB2 production of which the scientists state that

On a side note: The results of this study don't change my opinion as far as the usefulness, let alone necessity of fish oil supplementation in healthy, athletic, fish eating SuppVersity readers is concerned. I don't see any.

"[...]previous work by both Boughton-Smith et al. and Scott et al. suggest that PGE2, PGF2α, TXB2, and 6-keto-PGF1α are the primary products of the COX2 pathway when AA is in abundance. Furthermore, Scott and colleagues suggested that with chronic elevation of AA, PGF2α and TXB2 production is more likely to be up-regulated due to their vasoconstrictive qualities, which would prevent the efflux of AA and other more-damaging eicosanoids from cells into circulation." (Zulyniak. 2013)

Whether this is actually a good thing does yet appear at least somewhat questionable to me and even Zulyniak et al. have to admit that future research was necessary to confirm "the production of eicosanoids capable of regulating vasoconstriction" and thus "substantiate this hypothesis" (Zulyniak. 2013). As you can see, we are still learning new stuff about things of which every disciple of Dr Oz believes he already knew everything.

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Study supports hypothesis that regression in adipocyte size during weight loss could be reason for fat loss plateaus and "walls" (Verhoef. 2013) -- As a seasoned SuppVersity veteran, you are probably aware of the possible influence the size of your fat cells could have on weight loss success, failure or stagnation (learn more).

In a previous post on the Yoyo effect, I already discussed some aspects of adipocyte morphology - including the way lower body fat tends to be more stubborn than upper body fat (read more)

A recent study from the Maastricht University does now offer further support for my previously expressed hypothesis that the reduction of adipocyte size that comes with profound weight loss in then formerly obese individuals could be at the heart of the weight loss plateaus and over-pronounced metabolic downregulation formerly obese individuals experience at way higher body fat levels than someone who has never been obese in his / her whole life. Verhoef et al. put a group of twenty-eight overweight (BMI 28-35kg/m²) healthy subjects on a very low energy diet for 2 months. The 500kcal/day period (50g carbs, 52g protein, 7g fat + multi-mineral supplement delivering the RDA of all nutrients) was followed by a 10-month period of weight maintenance.

Over the course of the low energy diet intervention period, the adipocyte size decreased by -16.7%, the body fat level, on the other hand dropped by only 4.7%. Still, the leptin levels plummeted from 20.3 to 13.1 µg/L and did not return to baseline in the course of the "weight maintenance" phase.

Figure 2: Relative changes (compared to baseline) in body composition, adipocyte volume and leptin after the dieting intervention and the miserable weight maintenance phase (Verhoef. 2013)

In how far the suppressed leptin levels were actually responsible for the fact that the "weight maintenance" phase turned out to be a very dirty, fat only bulking phase cannot be said, but we know from previous studies, that the process of shrinking in itself

"has been reported to generate cellular stress and the more [the adipocytes] shrink, the higher will be the resistance against increasing mitochondrial beta-oxidation via HADHsc [hydroxyacyl-Coenzyme A dehydrogenase] during follow-up." (Verhoef. 2013)

And as if that was not enough the slight increase in ATGL (lipolytic protein) and HADHsc in the "weight maintenance" phase are, as the scientists point out, indicative of the appearance of newly differentiated adipocytes that are are metabolically active contribute to an "improved physiological status", but could potentially make future weight loss (esp. the aesthetic one) even more difficult.

"Empty" adipocytes <> lower leptin <> more glucose-to-fat conversion <> rapid fat gain

If CLA worked in humans as it does in rodents, it could solve the "small adipocyte" problem (learn why)

Moreover, the glycolyctic and thus potentially glucose-to-fat conversion promoting enzyme Aldolase-C did not just distinguish the successful weight maintainers (low Aldolase-C) from the yoyo dieters (high Aldolase-C), it also correlated with the leptin production of the fat cells, of which we know from previous studies that it is in turn negatively correlated to their size (Skurk. 2007)... too complicated?

Ok, let's express it the other way around. The "emptier" your adipocytes are (=smaller size), the less leptin they will produce and the more likely they are to convert glucose to fat and stash that away in their empty "tummies".

Suggested read for those who want to dig further into the purported underlying effects of weight regain: Maclean PS, Bergouignan A, Cornier MA, Jackman MR. Biology's response to dieting: the impetus for weight regain. Am J Physiol Regul Integr Comp Physiol. 2011 Sep;301(3):R581-600.

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That's it for an allegedly too lengthy installment of "On Short Notice"... about as much a misnomer as the "weight maintenance" phase in the Verhoef study, I guess. Maybe some of today's Facebook news can make up for that? In the end news like

Want to make HIIT a hit for you? Not a problem, the SuppVersity holds all the information you need. Start out with the respective two post article series and descend into the archives, where you are going to find more about HIIT, how it compares to LISS and which different regimen have shown some promise in peer-reviewed research (learn more)

• High fat dieting reduces the beneficial effects of resistant starch - Reduction in abdominal obesity with 42% fat diet = zero (read more)
• HIIT hits home in 8 young, untrained men - 12 HIIT sessions lead to increased V02 kinetics (read more)
• Ice slurries are the new energy gels - Scientists observe significant increases in cycling performance (read more)
• Physical therapy as effective as surgery for a meniscal tear and osteoarthritis - Unfortunately patients are too lazy and the revenue for the doctors too small to be used more often (read more)
• Evolution is to blame for inflammatory disease - At least that's what the latest "paleo" research would suggest (read more)

are eventually the reason that the saturdaily short news are always so lengthy. The really short stuff is already on Facebook ;-)

References:

• Gavrieli A, et al. Gender and body mass index modify the effect of increasing amounts of caffeinated coffee on postprandial glucose and insulin concentrations; a randomized, controlled, clinical trial. Metabolism.2013 [ahead of print]
• Pedersen DJ, Lessard SJ, Coffey VG, Churchley EG, Wootton AM, Ng T, Watt MJ, Hawley JA. High rates of muscle glycogen resynthesis after exhaustive exercise when carbohydrate is coingested with caffeine. J Appl Physiol. 2008 Jul;105(1):7-13.
• Verhoef SP, Camps SG, Bouwman FG, Mariman EC, Westerterp KR. Physiological response of adipocytes to weight loss and maintenance. PLoS One. 2013;8(3):e58011.
• Wyatt HR, Peters JC, Reed GW, Barry M, Hill JO. A Colorado statewide survey of walking and its relation to excessive weight. Med Sci Sports Exerc. 2005 May;37(5):724-30.
• Zulyniak MA, et al. Fish oil supplementation alters circulating eicosanoid concentrations in young healthy men. Metabolism. 2013 [ahead of print]

Working Out 45 Min After Dinner Improves Post-Meal Blood Glucose & Trigs More Effectively Than Working Out Before

Resistance training alone won't make up for a sloppy diet - no matter if you do it before or after meals.

I am not sure how feasible this is going to be for you, but if you are a type II diabetic or anyone concerned about the potential detrimental health effects of the rise in glucose and triglycerides after a meal, working out 45 minutes after dinner is the way to go.

Abnormally elevated postprandial glucose and triacylglycerol (TAG) concentrations are strong risk factors for cardiovascular disease (CVD) in patients with type-2 diabetes. Therefore, scientists expect that interventions that reduce postprandial glucose and TAG concentrations should lower the risk of CVD (Krook. 2003; O'Gorman. 2008).

Learn more about the effects of your diet on your health at the SuppVersity

Only Whey, Not Soy Works for Wheytloss

Taste Matters - Role of the Taste Receptors

Dairy Protein Satiety Shoot-Out: Casein vs. Whey

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5 Tips to Improve & Maintain Insulin Sensitivity

Carbohydrate Shortage in Paleo Land

Previous studies have shown that acute exercise typically lowers postprandial glucose and TAG concentrations (Tobin. 2008) in patients with type-2 diabetes, but as Timothy D. Heden et al. point out, there is considerable heterogeneity in the responses with some individuals not experiencing beneficial changes in these risk factors (Gill. 2007; van Dijk. 2012).

"One potential explanation why some patients with type-2 diabetes do not have beneficial changes in postprandial glucose and TAG with acute exercise is because of the timing of the acute exercise session relative to meal consumption. Limited evidence suggests that the timing of aerobic exercise around a meal may be important and might explain why some individuals are exercise “insensitive” or “non responders”." (Heden. 2014) 

The only study to directly compare the effect of pre-meal and post-meal aerobic exercise on postprandial glucose concentrations in patients with type-2 diabetes showed that post-dinner, but not pre-dinner walking, lowered postprandial glucose concentrations (Colberg. 2009).

Figure 1: Previous studies indicate that aerobic workouts after meals have more beneficial effects on the potentially unhealthy increases in glucose or triglycerides (Collberg. 2009)

Although no study has directly examined the effect of exercise timing on postprandial TAG in patients with type-2 diabetes, there is evidence that exercise performed the day prior to a high fat meal has no effect on postprandial TAG responses (Dalgaard. 2004; Gill. 2007), while post-breakfast aerobic exercise reduced the postprandial TAG response (Tobin. 2008). Taken together, it appears that aerobic exercise may have its most powerful effect to lower postprandial glucose and TAG responses when performed after a meal, possibly because of slowed gastric emptying and/or greater skeletal muscle glucose and TAG uptake and utilization at this time.

The question that remained was: Is the same true for resistance training?

Since resistance exercise (RE) has a more pronounced long(er)-lasting effect on ones metabolism than aerobic training, the researchers from the University of Missouri tested the hypothesis that post-dinner RE, compared to pre-dinner RE, would in fact be more effective at improving two clinically important postprandial risk factors (glucose and 109 TAG) for CVD at a time of day when they are typically highest in obese patients with type-2 diabetes.

The standardized test workout consisted of the following exercises (in this order): leg press, seated calf raises, seated chest flyes, seated back flyes, back extensions, shoulder raises, leg curls, and abdominal crunches. All exercises were performed for three sets (1-2 min rest between sets) of 10-repetitions for each RE. During this session, the first set for each exercise was a warm-up set and the weight used was 50% of the participants 10-RM. After the warm-up set, the weight for the next two sets was the participants previously determined 10-RM.

Figure 2: Postrandial lipid response in the obese type II diabetics (Heden. 2014)

As you can see in Figure 2 the scientists suspicion was right, the postprandial workout (M-RE) had significantly more pronounced beneficial effects on the lipid metabolism of the type II diabetic subjects who consumed a standardized breakfasts (English muffin, cheddar cheese, one large egg, ham, hash brown, ketchup, and apple or orange juice) lunch (white bread, ham, mayonnaise, cheddar cheese, a granola bar, and apple or orange juice) and dinner meals (spaghetti noodles, spaghetti sauce with beef added, garlic bread, a lemon lime flavored soda, and 1.5 g of acetaminophen (to assess gastric emptying)) containing ~50% carbohydrate, 35% fat, and 15% protein.

Similar effects were observed for the insulin and glucose responses (see Figure 3) which were significantly improved and should thus complement the beneficial effects of the reduced triglyceride and very low density lipoprotein (VLDL) levels.

Figure 3: Changes in postprandial insulin and glucose levels (Heden. 2014)

Bottom line: Before we get to the actual interpretation of the result let me briefly point out that it would probably have been at least as effective if the subject had not been fed bull**** like ketchup, mayonnaise, granola bars, and purportedly healthy, but de facto obesogenic fruit juices. The unfortunate truth, however, is that 99% of the type II diabetics still eat like this. For them, the use of resistance training after each meal may be a possible, but unquestionably not practical way to ameliorate the unwanted cardiovascular side effects.

In view of the fact that most diabetics don't work at all, I am 100% convinced that the results of the study at hand have zero practical significance - even I wouldn't go work out after dinner only to lie in bed hungrily, thereafter, And if I did, I would raid the fridge later at night - certainly not a practice that's heart healthier than working out before dinner.

Speaking of which: Working out before dinner would also mean working out after lunch and could thus effectively help the increase in triglycerides and glucose after lunch. Not too bad either, right? | Comment on Facebook!

References:

• Colberg, Sheri R., et al. "Postprandial walking is better for lowering the glycemic effect of dinner than pre-dinner exercise in type 2 diabetic individuals." Journal of the American Medical Directors Association 10.6 (2009): 394-397. 
• Dalgaard, Marian, Claus Thomsen, and Kjeld Hermansen. "Effects of one single bout of low-intensity exercise on postprandial lipaemia in type 2 diabetic men." British Journal of Nutrition 92.03 (2004): 469-476.
• Gill, Jason MR, et al. "Effect of prior moderate exercise on postprandial metabolism in men with type 2 diabetes: heterogeneity of responses." Atherosclerosis 194.1 (2007): 134-143.
• Heden, Timothy D., et al. "Post-dinner resistance exercise improves postprandial risk factors more effectively than pre-dinner resistance exercise in patients with type 2 diabetes."
  Journal of Applied Physiology (2014). Ahead of print.
• Krook, Anna, et al. "Reduction of risk factors following lifestyle modification programme in subjects with type 2 (non‐insulin dependent) diabetes mellitus." Clinical physiology and functional imaging 23.1 (2003): 21-30.
• O'Gorman, Donal J., and Anna Krook. "Exercise and the treatment of diabetes and obesity." Endocrinology and metabolism clinics of North America 37.4 (2008): 887-903.
• Tobin, L. W. L., Bente Kiens, and Henrik Galbo. "The effect of exercise on postprandial lipidemia in type 2 diabetic patients." European journal of applied physiology 102.3 (2008): 361-370.
• van Dijk, Jan-Willem, et al. "Exercise and 24-h glycemic control: equal effects for all type 2 diabetic patients?." Medicine and science in sports and exercise (2012).