We've long understood that fat is the body's principal energy-storage tissue. However, it's now becoming clear that fat tissue is a major hormone-secreting organ, producing cell-signaling proteins called adipokines that play an important role in metabolism, feeding behaviors, glucose regulation and insulin control (Singla, Bardoloi & Parkash 2010; Al-Suhaimi & Shehzad, 2013).
Scientists know a lot about how fat affects our metabolism. They're also gleaning new insights on the FTO (fat mass and obesity associated) gene, on being "fat and fit," on the effects of extreme exercise and dieting programs, and on weight regain after intentional weight loss. Let's look at all these issues in more detail.
Adipokines: Leptin, Adiponectin and Visfatin
How does fat affect our body's biology? For starters, white-fat tissues under the skin (subcutaneous) and near the bodily organs (visceral) secrete messenger molecules called adipokines (Kwon & Pessin 2013). These molecules form biologically active proteins that are deeply involved in food intake, fat storage, metabolic disorders, and pro- and anti-inflammatory processes (Al-Suhaimi & Shehzad 2013).
Adipokines communicate with the liver, brain, muscles, immune system and other fat tissues (Kwon & Pessin 2013). Three adipokines are notable for fitness pros: leptin, adioponectin and visfatin.
Here's why each of them matters:
Leptin, whose name derives from the Greek leptos (meaning thin), has several roles in the body, including growth, immune system regulation and insulin sensitivity control (Al-Suhaimi & Shehzad 2013; Singla, Bardoloi & Parkash 2010). Leptin is one of a group of proteins secreted by fat tissue that help control body weight by regulating our metabolism.
Leptin is directly involved in triggering our decision to have a snack, which is referred to as a metabolic behavior. This makes leptin essential in regulating energy expenditure and controlling appetite. Obese people have been found to have elevated leptin levels in their blood plasma (Paracchini, Pedotti & Taioli 2005), accompanied by reduced leptin action in the brain. While this dysfunction is intriguing, it's unclear whether it actually causes obesity (Singla, Bardoloi & Parkash 2010). Future studies will have to figure that out.
Adiponectin helps to regulate metabolic homeostasis (or balance). This molecule is involved in insulin sensitivity enhancement, anti-inflammatory effects, and protection against atherosclerosis (Al-Suhaimi & Shehzad 2013). In lean people, adiponectin levels are high, which has been shown to improve liver insulin actions and glucose uptake in skeletal muscle and the liver (Singla, Bardoloi & Parkash 2010). Adiponectin also helps to protect blood vessels (Singla, Bardoloi & Parkash 2010).
Singla and colleagues note that the production and concentration of adiponectin in the blood decrease as people become obese. This may help explain why the low levels of adiponectin associated with obesity accompany increased risk of cardiovascular damage (Singla, Bardoloi & Parkash 2010).
Visfatin is an adipokine protein hormone that is elevated when abdominal obesity and type 2 diabetes are present (Beltowski 2006). Visfatin, produced by visceral fat, stimulates the maturation of pre-adipocytes to mature fat cells, induces the accumulation of triglyceride (a stored form of fat in the body) and accelerates triglyceride synthesis from glucose.
Beltowski notes that the higher visfatin levels observed with obesity may reflect the body compensating to maintain blood glucose. This suggests that visfatin exerts a beneficial glucose-lowering effect by stimulating glucose utilization in peripheral tissues (Beltowski 2006). While it looks like visfatin protects against obesity-related pathologies, more research is needed to determine whether this adipokine can be used to treat obesity (Beltowski 2006).
New Insights on the FTO Gene and Physical Activity
In 2007, a large study of over 38,000 Europeans identified the FTO gene and its link to a predisposition to diabetes and obesity (Frayling et al. 2007). Until recently, there had been little research on the effect of physical activity on the FTO gene (see Figure 2), but that changed this year with the publication of the Food4me study (Celis-Morales et al. 2016), which has profound implications for personal trainers.
Working with 743 women and 537 men (average age of 40), Celis-Morales and colleagues collected physical activity data with accelerometers for 2 weeks. The study found that people achieving between 10 and 90 minutes of vigorous physical activity per week alleviated the FTO genotype's effect on obesity measures. By contrast, people needed 150–300 minutes of moderate-intensity exercise to reduce the association between the FTO genotype and obesity.
The take-home message: Physical activity is effective at managing body weight in people with a genetic predisposition for obesity—contradicting the deterministic view that we cannot do anything about the genetic influences on obesity.
New Insights on "Fat but Fit"
Medical science is growing more interested in the idea of being fat but fit. This, in turn, is an important consideration for exercise professionals. Després (2015) says we must note that most people in the fat-but-fit category are in the overweight/moderate-obesity range—they are not those with extreme obesity. Fat-but-fit people have less visceral fat tissue (see Figure 1) for a given body mass index than fat-but-unfit people. Additionally, Després notes that several lifestyle-modification studies that have incorporated an endurance exercise program have shown it can induce a selective loss of both abdominal fat and fat around the heart with no change in body weight.
Finally, Després emphasizes that changing from sedentary behavior to a physically active lifestyle has been shown to turn on the expression of numerous genes for proteins involved in structural, physiological and metabolic adaptations. These changes provide cardio-protection, irrespective of weight loss.
The take-home message (important to emphasize to clients): Striving for better health may be preferable to struggling for an unattainable "model" figure.
Follow-Up on "Dieting Makes You Fat! How?"
In our previous column, we reported on a study of 14 Biggest Loser contestants (6 men, 8 women) who in the 6 years after the show regained a substantial amount of the weight they'd lost in the 30-week exercise/nutrition intervention (Kravitz 2016).
Surprisingly, at the 6-year follow-up, the participants' resting metabolic rates were dramatically suppressed (Kravitz 2016). (These findings generated heated discussions at the 2016 IDEA® World Convention in Los Angeles.) Many fitness pros and exercise scientists note that the research clearly shows the harm of trying to lose massive amounts of weight unnaturally with extreme exercise and dieting.
The take-home message: Gradual, reasonable weight loss leads to developing new, healthy behaviors that prevent weight regain.
New Insights on Abnormal Hormone Levels After Intentional Weight Loss
Stohacker and colleagues (2014) completed a systematic review of studies that assessed changes in leptin, ghrelin (a potent appetite-stimulating hormone) and insulin sensitivity during weight loss, and tested the relationship between such changes and weight regain. In clinical weight loss trials, according to the review, neither decreases in leptin or insulin sensitivity nor increases in ghrelin reliably predicted subsequent weight regain.
Stohacker et al. proposed that future investigations need to determine if there is a "conglomerate effect" of several hormones (including leptin, ghrelin, insulin, peptide YY, cholecystokinin, amylin and glucagon-like peptide-1) on weight regain. For now, the researchers suggest we focus on changing the environments that promote weight gain (called obesogenic environments). These environments, which are common worldwide, feature a dearth of opportunities for activity, with few walkways or cycle paths for recreation; fast-food temptations everywhere; an abundance of sugar-sweetened beverages, pastries and desserts; and large portion sizes at most restaurants.
With so much new research and new understandings on fat, one message leads the way for fitness professionals: Changing from a sedentary behavior to a physically active lifestyle has enormous health benefits. Start moving, and keep moving!
Al-Suhaimi, E.A., & Shehzad, A. 2013. Leptin, resistin and visfatin: The missing link between endocrine metabolic disorders and immunity. European Journal of Medical Research,18, 12.
Beltowski, J. 2006. Apelin and visfatin: Unique “beneficial” adipokines upregulated in obesity? Medical Science Monitor, 12 (6), RA112-19.
Celis-Morales, C., et al. 2016. Physical activity attenuates the effect of the FTO genotype on obesity traits in European adults: The Food4Me study. Obesity, 24 (4), 962-69.
Despr├®s, J.-P. 2015. Obesity and cardiovascular disease: Weight loss is not the only target. Canadian Journal of Cardiology, 31 (31), 216-22.
Frayling, T.M., et al. 2007. A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity. Science, 316 (5826), 889-94.
Kravitz, L. 2016. Dieting makes you fat! How? IDEA Fitness Journal, 13 (8), 16-19.
Kwon, H., & Pessin, J.E. 2013. Adipokines mediate inflammation and insulin resistance. Frontiers in Endocrinology, 4, article 71, 1-9.
Paracchini, V., Pedotti, P., & Taioli, E. 2005. Genetics of leptin and obesity: A HuGE review, American Journal of Epidemiology, 162 (2), 101-14.
, A.-L., et al. 2015. Brown adipose tissue activity as a target for the treatment of obesity/insulin resistance. Frontiers in Physiology, 6, article 4.
Singla, P., Bardoloi, A., & Parkash, A.A. 2010. Metabolic effects of obesity: A review. World Journal of Diabetes, 1 (3), 76-88.
Stohacker, K., et al. 2014. Adaptations of leptin, ghrelin or insulin during weight loss as predictors of weight regain: A review of current literature. International Journal of Obesity, 38, /i> 388-96.