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How Your Gut Tastes What You Eat

sharma-obesity-guthormones2If you thought that the only senses that determine the palatability of food are your sense of taste and smell, you may be wrong.

It turns out that we have a rather sophisticated sensing mechanism in our gut that senses the composition of our diet and interacts with the brain to regulate our appetite and food intake.

Just how exactly this gut “nutrient-sensing” system works, is reviewed by Sophie Hamr and colleagues from the University of Toronto in a paper published in Current Diabetes Reports.

As the authors point out,

“…the gastrointestinal (GI) tract is anatomically positioned to provide initial feedback following a meal via detection of incoming nutrients and relaying signals to the brain and peripheral tissues to prevent excess energy intake and circulating nutrients…..This, coupled with the vast neural and humoral connectivity of the gut to other important sites of energy regulation, such as the brain, allows the gut to effectively relay information to the rest of the body about the size and composition of an incoming meal.”

Each nutrient (fats, carbohydrates, protein) interacts with specific sensory and signal transduction mechanisms in the gut.

Animal studies show that exposing the gut to certain nutrients (for e.g. by tube feeding) can stimulate or suppress feeding behaviour making animals chose or avoid certain foods. Often these effects can persist for days or even weeks, well beyond the time course of a single meal.

Furthermore, these effects appear to be largely dependent on the presence of specific nutrients rather than on the actual nutritional or energy state of the animal.

“…these evidences lend notion for the intestine to sense specific nutrients (i.e., lipid and carbohydrate) at specific concentrations, rather than calories, in an effort to drive further food consumption.”

The authors point out that changes in how the gut senses nutrients may well explain how bariatric surgery works to reduce appetite and change food preferences.

No doubt, a better understanding these mechanisms and the molecular mechanisms involved could lead to novel dietary or pharmacological interventions to prevent or treat obesity.

@DrSharma
Edmonton, AB

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Post-Weight Loss Fat Gain in US Rangers

army-rangersAnd finally, to conclude this week’s discussion of evidence to support the notion that weight cycling predicts weight (fat) gain especially in normal weight individuals, I turn back to the paper by Dulloo and colleagues published in Obesity Reviews, which quotes these interesting findings in US Rangers:

“…U.S. Army Ranger School where about 12% of weight loss was observed following 8–9 weeks of training in a multi-stressor environment that includes energy deficit. Nindl et al. reported that at week 5 in the post-training recovery phase, body weight had overshot by 5 kg, reflected primarily in large gains in fat mass, and that all the 10 subjects in that study had higher fat mass than before weight lost. Similarly, in another 8 weeks of U.S. Army Ranger training course that consisted of four repeated cycles of restricted energy intake and refeeding, Friedl et al. showed that more weight was regained than was lost after 5 weeks of recovery following training cessation, with substantial fat overshooting (∼4 kg on average) representing an absolute increase of 40% in body fat compared with pre-training levels. From the data obtained in a parallel group of subjects, they showed that hyperphagia peaked at ∼4 weeks post-training, thereby suggesting that hyperphagia was likely persisting over the last week of refeeding, during which body fat had already exceeded baseline levels.”

Obviously, association (even in a prospective cohort) does not prove causality or, for that matter, provide insights into the physiological mechanisms underlying this observation.

All we can conclude, is that these observations in US Rangers (and the other studies cited in Dulloo’s article) are consistent with the notion that weight loss in normal weight individuals can be followed by significant weight gain, often overshooting initial weight.

Incidentally, these findings are also consistent with observational studies in women recovering from anorexia nervosa, famine, cancer survivors and other situations resulting in significant weight loss in normal weight individuals.

Certainly enough evidence to consider a work of caution against “recreational” weight loss, especially in individuals of normal weight.

@DrSharma
Edmonton, AB

ResearchBlogging.orgDulloo AG, Jacquet J, Montani JP, & Schutz Y (2015). How dieting makes the lean fatter: from a perspective of body composition autoregulation through adipostats and proteinstats awaiting discovery. Obesity reviews : an official journal of the International Association for the Study of Obesity, 16 Suppl 1, 25-35 PMID: 25614201

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Did Dieting Make You Fat? Blame Your ‘Proteinstat’

Skeletal muscle

Skeletal muscle

Yesterday, I posted on the intriguing finding (now documented in 15 prospective studies) that dieting can make you fat – especially if you start out with a normal weight.

In the paper by Dulloo and colleagues published in Obesity Reviews, the authors attribute part of this effect to the so far elusive “proteinstat” – a system, similar but different from the “adipostat” – that is designed to protect your lean body mass.

As the paper nicely delineates, the problem with post-dieting weight regain is that the fat comes back first but that the drive to eat does not cease till you have also regained the lost lean body mass (muscle).

It appears as though there are two complimentary biological systems that regulate weight regain.

The better known system is the “adipostat” that worries about protecting and restoring fat mass – the neuroendocrine players include leptin and perhaps other signals derived from fat tissue that signal fat stores to the brain. This system works (primarily through dropping metabolic rate but also through effects on appetite) to very quickly and effectively restore the depleted fat mass after dieting.

The less known system is the “proteinstat”, that apparenty worries about restoring lean body mass. The system works slower than the “adipostat” but continues its activity (often reaching its peak) even after all the lost fat has been regained and you are back to your original weight. In fact, it continuous working (primarily through appetite and cravings) till lean body mass is restored, even if this means gaining even more fat in the process.

In their careful reanalysis of starvation studies, Dulloo and colleagues also come up with an explanation why this process of “weight overshoot” results in more gain the skinnier the individual is to begin with.

“…the lower the initial adiposity, the greater the proportion of energy mobilized as body protein (referred to as P-ratio) during weight loss. The steep part of the negative exponential curve lies between 8–20% body fat, and a shift from the upper to the lower values in this range, generally considered to reflect a ‘normal’range of adiposity for men living in affluent societies, results in 2.5- to 3-fold increase in the P-ratio; the latter constitutes a proxy of the fraction of weight that is lost as FFM since protein belongs to the FFM compartment. This extremely high sensitivity of the P-ratio with regard to the initial body composition emphasizes the critical importance of even small differences in the initial percentage body fat in dictating the individual’s energy-partitioning characteristic and, hence, the pattern of lean and fat tissue deposition during weight loss and subsequent
weight regain, in turn, determining the extent of fat overshooting.”

In other words, lean dieters are far more susceptible to mobilising energy (and thus losing mass) from their muscle than from their fat stores, resulting in a much greater likelihood of overshooting their original weight.

Eventually, as these dieters get fatter with every diet cycle, they get less and less susceptible to this effect, which matches well with the finding that dieting is a far better predictor of long-term weight gain in people with lower fat percentages than in those who already have overweight or obesity).

As for exactly how the “proteinstat” works, much remains unclear. Early work focussed on the notion that certain amino acids may serve as signals of protein stores, however, now work is focussing on the far more plausible theory that some of the over 100 molecules now known to be secreted by skeletal muscle (myokines) may play a role in this system.

Certainly a topic that will be interesting to watch develop over the coming years.

@DrSharma
Calgary, AB

ResearchBlogging.orgDulloo AG, Jacquet J, Montani JP, & Schutz Y (2015). How dieting makes the lean fatter: from a perspective of body composition autoregulation through adipostats and proteinstats awaiting discovery. Obesity reviews : an official journal of the International Association for the Study of Obesity, 16 Suppl 1, 25-35 PMID: 25614201

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Type 1 Plus Type 2 diabetes Is Not Type 3 Diabetes?

sharma-obesity-brainLast week at the 8th Annual Obesity Symposium hosted by the European Surgery Institute in Norderstedt, one of the case presentations included an individual with type 1 diabetes (no insulin production), who had gained weight and subsequently also developed increasing insulin resistance, the hallmark of type 2 diabetes.

In my discussion, I referred to this as 1+2 diabetes, or in other words, type 3 diabetes.

Unfortunately, it turns out that the term type 3 diabetes has already been proposed for the type of neuronal insulin resistance found in patients with Alzheimer’s disease.

As discussed in a paper by Suzanne de la Monte and Jack Wands published in the Journal of Diabetes Science and Technology,

“Referring to Alzheimer’s disease as Type 3 diabetes (T3DM) is justified, because the fundamental molecular and biochemical abnormalities overlap with T1DM and T2DM rather than mimic the effects of either one.”

These findings have considerable implications for our understanding of Alzheimer’s disease as a largely neuroendocrine disorder, which may in part be amenable to treatment with drugs normally used to treat type 1 and/or type 2 diabetes.

In retrospect, I believe, whoever came up with the term type 3 diabetes for Alzheimer’s disease, should perhaps have called it type 4 diabetes, given that the 1+2 diabetes is now increasingly common (and well studied) in patients with type 1 diabetes, who go on to develop type 2 diabetes (which, as discussed at the symposium responds quite well to bariatric or “metabolic” surgery).

@DrSharma
Edmonton, AB

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Exercise Reduces Cravings For Sugar?

sharma-obesity-exercise2I have long postulated that the benefits of exercise in weight management have little to do with burning calories. Rather, I am pretty sure that when people lose weight with exercise, they do so because of the impact that exercise may have on their food intake (I call it exercising to ruin your appetite!).

Thus, I am happy to acknowledge my affirmation bias in paosting about the recent study by Larissa Ledochowski and colleagues from the University of Innsbruck, Austria, published in PLOS One on the outcome of a randomised controlled trial of brisk walking on cravings for sugary snacks.

The study was conducted in 47 overweight volunteers who reported habitually consuming a fair share of sugary snacks. Following 3 days of “chocolate abstinence” subjects were randomised (using a within-subject design) to a 15-min brisk walk or passive control.

On each occasion, subjects were then stressed using the Stroop color–word interference task after which they reported their urges for sugary snacks using the State Food Craving Questionnaire [FCQ-S] adapted for sugary snacks.

Compared to the control situation, brisk walking resulted in a significant and relevant reduction in the urge for sugary snacks and attenuated the increase in sugar-cravings under trigger conditions (stress).

Although the authors are careful about not over-interpreting their findings from this acute study (that did not actually measure sugary-snack intake), they do make the following speculation regarding clinical relevance,

“This study adds to the increasing evidence that physical activity can somehow help to regulate the urge to consume snack food. It may be easy for overweight people to fit in short bouts of low-moderate intensity physical activity, instead of being sedentary, to elevate affective activation and valence and reduce high energy food cravings which may be triggered by stress and the presence of snack foods.”

While I am certain that more intense exercise may well trigger a hunger response, it appears that even a short bout of brisk walking may help dispel those cravings for sugary snacks (let me know if you have experienced this).

@DrSharma
Edmonton, AB

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