One last cupcake sounds awfully
good at this moment right? If you
answered yes this could mean that you have a low level of leptin floating in
your blood. Leptin is a hormone that signals to the brain when you are full. So
when leptin levels are high you begin to feel satisfied and your body begins to
utilize some of the fat for energy. The amount secreted is typically
proportionate to the amount of fat distributed on a person’s body but with
humans, there are always complications. People with a higher body fat content
have a higher level of leptin in their blood however, some individuals may be
resistant to leptin or maintain a higher threshold of it, which therefore leads
to obesity.
If leptin is
a hormone that curbs hunger how can it commence lipolysis? One study found
while using a complex microscopy technique that sympathetic nerve fibers act
directly on fat cells allowing the brain to communicate with fat. So when in a
stressful situation the brain is able to use the energy stores from fast
instantly and eventually bring the body back to homeostasis. But what about the
people who may be resistant to leptin or lack the adequate amount of direct
sympathetic fibers to control their fat levels?
Another
study found that two neuropeptides, B and W, through a g-protein coupled
receptor, GPR7, could have vital effects on lipolysis and leptin levels in rats.
They found that both of the neuropeptides, when activated through GPR7,
actually reduced leptin levels in the rats and adversely amplified lipolysis.
This means that they found a way to neurologically activate a way to get rid of
fat without having to increase leptin levels. Their findings may arise some unknown
steps that these neuropeptides have on mobilization of energy and appetite in
rodents.
Leptin is
one of the great biological developments that has helped to regulate weight and
control fat content in humans and other mammals. The current advancements in
research on this might open up some doors for creating new drugs that could
reduce the obesity rate in the U.S. as well as a better understanding as to how
leptin and lipolysis are intertwined. Nevertheless could it also lead the way
to a lazier, get thin fast society?
Skrzypski, M.,
Pruszyńska-Oszmałek, E., Ruciński, M., Szczepankiewicz, D., Sassek, M.,
Wojciechowicz, T., & ... Nowak, K. W. (2012). Neuropeptide B and W regulate
leptin and resistin secretion, and stimulate lipolysis in isolated rat
adipocytes. Regulatory Peptides, 176(1-3), 51-56.
doi:10.1016/j.regpep.2012.03.004
Zeng, W.,
Pirzgalska, R. M., Pereira, M. M., Kubasova, N., Barateiro, A., Seixas, E.,
& ... Domingos, A. I. (2015). Sympathetic Neuro-adipose Connections Mediate
Leptin-Driven Lipolysis. Cell, 163(1), 84-94. doi:10.1016/j.cell.2015.08.055
Wouldn't this be nice! An easy way to break down fat simply through neuropeptides would seemingly be a huge advancement in the treatment of obesity. Currently there are ways in which weight loss can be achieved but they are not easy, like having dietary restrictions, exercising regularly, and even counseling has been shown to help. There are also medications to help with weight loss, however there should be a combination of all listed treatments to show the most improvement.
ReplyDeleteAnother interesting treatment I saw was vagus nerve blockade. The vagus nerve innervates several abdominal organs such as the stomach. With this technique there is an electrode implanted on this nerve that sends a "I'm full" signal to the brain, therefor reducing food intake and eventually leading to weight loss.
http://www.mayoclinic.org/diseases-conditions/obesity/basics/treatment/con-20014834
I thought this article group up a really interesting point about how being thin is the norm in our society these days. So when our nerve fibers act directly on fat cells and direct lipolysis, is there something that can interfere with this process? For example, when people drink diet supplementary, how does that work? I was wondering since our brain is the one that signals for lipolysis? how does diet pills or other supplementary works?
ReplyDeleteVery interesting post! Indeed, the dietary patterns of our society have resulted in an increased prevalence of obesity. The way we view eating has changed drastically since the days of hunters and gatherers – we are often planning out our next meals without feeling hungry. Could our bodies be secreting more and more ghrelin – the hunger hormone? Or are we becoming less and less response to the satiety hormone – leptin? Perhaps, the neurological connections between the brain and adipose cells have become weaker and weaker, causing problems with controlling the amount of fat in our bodies.
ReplyDeleteAs the rate of obesity-related diseases continues rising, the search for a “cure” goes on. I found it very interesting how the two neuropeptides, B and W, have the potential to increase leptin levels and catalyze lipolysis. However, if the problem is deceased sensitivity to leptin, then increasing the levels of this hormone won’t necessarily solve the problem. This research is likely the beginning of a movement to cure the problem of obesity, but I still believe that monitoring our diets and exercising regularly will be the most effective methods. Overall, by better understanding the causes of obesity in our society, we can work to develop cures, treatments, and programs to reduce the levels of obesity and return people to their proper healthy states.
While I agree that dietary patterns is a major influence on the increased prevalence of obesity in our society, I believe that it is our shift towards a more sedentary lifestyle that is the more important factor. Studies show that exercise actually reduces the leptin concentration in the blood (Martins et al., 2013). This means that the receptors would be up-regulated during exercise, increasing the sensitivity of the receptors to leptin instead of the decreased sensitivity found within the obese populations in the studies above. This is why I see that using leptin as a weight loss drug would be problematic because it is the excess of leptin in individuals suffering from obesity that causes the decreased sensitivity resulting lower levels of lipolysis. However, while the neuropeptides B and W act in a way that is similar to exercise,meaning it decreases letpin levels to increase later sensitivity, i believe as a drug it could be abused. For example if one wanted to lose weight quickly they might take a large amount of the drug which would not only reduce the amount of leptin in the blood hindering lipolysis they would also be hindering their satiety drive which would cause them to binge eat without the benefit of being able to burn their fat stores resulting in massive weight gain (causing a vicious cycle). While i believe that we have made great progress in understanding obesity and its underlying factors, I do not think that just because we think we might have found a 'cure' that we should jump to conclusions about its use in the general population without fully understanding how it works and how it could possibly be abused.
DeleteReferences
Martins, C., Kulseng, B., Rehfeld, J. F., King, N. A., & Blundell, J. E. (2013). Effect of chronic exercise on appetite control in overweight and obese individuals. Medicine And Science In Sports And Exercise, 45(5), 805-812. doi:10.1249/MSS.0b013e31827d1618
Another interesting factor implicated in leptin regulation and obesity is one's circadian rhythms. The sleep-wake cycle of an individual is closely linked to hypothalamic activation, lipogenic pathways, and overall metabolism. Leptin (and ghrelin) are released on a 24-hour cycle, with leptin secretions peaking during sleep (i.e., fasting stage), which causes to increased satiety and increased metabolism, as you point out. What interests me is the effect altered sleep patterns then have on leptin release. If, for instance, one extends their wake cycle (take your pick from any sleep-deprived college student), the release of leptin may be decreased, ultimately decreasing satiety and metabolic activity. This is definitely an interesting complication to the hormonal control of the obesity problem (see review by Froy, 2009).
ReplyDeleteFroy, O. (2010). Metabolism and circadian rhythms—implications for obesity. Endocrine reviews, 31(1), 1-24.
Another interesting factor implicated in leptin regulation and obesity is one's circadian rhythms. The sleep-wake cycle of an individual is closely linked to hypothalamic activation, lipogenic pathways, and overall metabolism. Leptin (and ghrelin) are released on a 24-hour cycle, with leptin secretions peaking during sleep (i.e., fasting stage), which causes to increased satiety and increased metabolism, as you point out. What interests me is the effect altered sleep patterns then have on leptin release. If, for instance, one extends their wake cycle (take your pick from any sleep-deprived college student), the release of leptin may be decreased, ultimately decreasing satiety and metabolic activity. This is definitely an interesting complication to the hormonal control of the obesity problem (see review by Froy, 2009).
ReplyDeleteFroy, O. (2010). Metabolism and circadian rhythms—implications for obesity. Endocrine reviews, 31(1), 1-24.
This is a really interesting topic. As I was reading, I started wondering what different food intakes might due to the leptin response. A study published on the American Diabetes Association website, investigated the effects of high fat meals on leptin levels in women. Insulin responses to meals create a related nocturnal increase of leptin levels, therefore they hypothesized that high fat, low carb vs low fat, high carb meals would create a lowered insulin, and therefore leptin response. As mentioned early leptin is involved in adipocyte glucose utilization, which can mean detrimental effects to a person’s weight control if leptin is not operating optimally. This study found that a high fat, low carb meals leptin responses were indeed significantly lower than following a low fat/ high carb meal. The high fat meals even lowered nocturnal leptin release. So if you are craving that extra cupcake, it might be wise to choose one with a low-fat icing to forego additional weight gain!
ReplyDeleteLink to article: http://diabetes.diabetesjournals.org/content/48/2/334.short