You may not exactly like the things you learn about fat in today’s post, but fat seems to be society’s public enemy number one lately, and you know what they say — it’s always best to know your enemy.

Here’s a fat cell:

It’s relatively huge as far as cells go. With a diameter of about a tenth of a millimeter, it’s over 100 times the size of a skin cell, and just one fat cell is potentially visible by the naked eye. As you can see, most of a fat cell is a huge pool of fat, with all of the other parts of the cell squished off to the side. If you’re the average adult, you’ve got about 30 billion of these guys. All the more reason to know what they’re capable of, right?

1. Fat cells can pilfer your medications and vitamins. At the most basic level, when you take medicine or vitamins, your body uses what you need and the byproducts or whatever your body doesn’t use are excreted. However, many vitamins (like A, D, E, and K) and medications (including many antidepressants and anesthetics) are fat-soluble, as opposed to water-soluble, meaning that as they circulate your body they can slip out of your blood and into your fat. THC, the active compound in marijuana, is an example of a fat-soluble drug; if an obese person with large amounts of body fat gets high with a skinny person with low levels of body fat, it is likely that the obese person would test positive for a longer stretch of time, because the obese person has more fat cells to trap the THC and release its metabolites more slowly over time.

Sneaky fat cells…

2. Fat cells influence how hungry you are and whether or not you get diabetes and heart disease. As it turns out, fat cells don’t just take stuff out of your blood, they put stuff in it, too. In particular, fat cells make a whole bunch of hormones and inflammatory molecules. One of the most important molecules made by fat is leptin, which signals to the brain and decreases appetite. Mice without receptors for leptin become obese:

Fat tissue also releases inflammatory molecules called cytokines that can decrease the ability of the body to respond to insulin, which can set the stage for diabetes. Some of these inflammatory molecules are also thought to promote systemic inflammation, and research suggests that this can make atherosclerosis (artery blockage due to fat accumulation) all the more dangerous. That’s because inflammatory cells might be able to rupture atherosclerotic buildup, creating clots that induce heart attacks or strokes.

This is a lot of information to take in, and the many roles of fat as a signaling tissue make up a very active area of research right now, especially because fat can often turn on or off production of specific molecules in obese individuals.

3. Fat cells can feed cancer cells. If you weren’t hating fat by now, this might just tip the scales. Very recent research in Nature Medicine suggests that abdominal cancers, like ovarian cancer, are made worse by fat. Ovarian cancers tend to metastasize to fat-dense regions of the abdomen, and fat cells can directly transfer fat to cancer cells, which provides the cancer with energy and allows it to grow in size.The silver lining of these findings is that researchers may now have a new mechanism to target when designing drugs to fight cancers that flourish in fatty areas of the body.

4. Fat cells might be the cure to just about everything. Alright, last but not least, a major redeeming feature of fat: it’s got stem cells in it. In general, stem cells are cells that have the potential to differentiate into multiple other cell types. Scientists have theorized stem cells to be a potential therapy for just about every disease condition (e.g. using stem cell-derived neurons to replace the lost/damaged neurons in neurodegenerative diseases). Although fat stem cells can’t turn into as many cell types as embryonic stem cells can, they have many upsides: fat stem cells circumvent ethical concerns, are readily available thanks to all of the fat-removing surgeries done today, and pose far less risk of immune rejection when re-introducing cells taken from someone’s own fat. Fat stem cells have already been shown to essentially cure a mouse model of lupus.

So maybe you’re not necessarily any happier about your fat now, but I hope you have a new appreciation for it. While you lament your muffin top, you can consider the diverse biology of your muffin top. That might sound nerdy, but…well, that’s the whole point.

Ovchinnikova O, Robertson AK, Wågsäter D, Folco EJ, Hyry M, Myllyharju J, Eriksson P, Libby P, & Hansson GK (2009). T-cell activation leads to reduced collagen maturation in atherosclerotic plaques of Apoe(-/-) mice. The American journal of pathology, 174 (2), 693-700 PMID: 19131590

Nieman KM, Kenny HA, Penicka CV, Ladanyi A, Buell-Gutbrod R, Zillhardt MR, Romero IL, Carey MS, Mills GB, Hotamisligil GS, Yamada SD, Peter ME, Gwin K, & Lengyel E (2011). Adipocytes promote ovarian cancer metastasis and provide energy for rapid tumor growth. Nature medicine, 17 (11), 1498-503 PMID: 22037646

Choi EW, Shin IS, Park SY, Park JH, Kim JS, Yoon EJ, Kang SK, Ra JC, & Hong SH (2011). Reversal of serological, immunological and histological dysfunction in systemic lupus erythematosus mice by long-term serial adipose tissue-derived mesenchymal stem cell transplantation. Arthritis and rheumatism PMID: 21904997

Probably wasn't grown in a lab.

I love eating meat. It’s no secret that I would probably be strictly carnivorous if it were just as easy to whip up a half-rack of ribs as it is to pour a bowl of cereal. Alas, meat preparation can be relatively involved, so I don’t eat it with every meal. But I do get what I call “protein deprivation” headaches if I have to go more than, say, 24 hours without meat.

All of this is to say that I have a vested interest in knowing I have a reliable supply of meat of available. So I wish I would’ve been less, um, nauseated when I learned how serious scientists are about lab-grown meat meat as the smart alternative to the real deal.

Warning: I apologize upfront to any vegetarians, vegans, or anyone else who takes offense to my undying love of meat. I am flawed.

Let’s start out with a poll, just because I’m curious:

Despite my love of science and nerdy things, I must admit I’m in the category of “Never! The concept of it makes me lose my appetite!” I’m just being honest, and I imagine I’m not the only person whose mouth fails to water at the image of some researcher growing meat on a plate somewhere in an almost science-fiction-gone-real scenario. My mouth doesn’t water at the idea of slaughterhouses either, but I can’t shake the feeling that the meat I eat should come from a full-fledged animal and not from tissue growing in an incubator.

But I’m getting ahead of myself. The latest discussions on in vitro meat production come out of a recent workshop in Gothenburg, Sweden focusing on the exploration of cultured meat. Some of the benefits (many environmental) of cultured meat could include:

- Reduction of greenhouse gas emissions. Farm animals grazing around emitting methane from their rear ends contribute quite a bit to the greenhouse gas problem, and using cultured meat in place of traditional meat could reduce these emissions.

- Increased land and water resources if fewer animals were grown for meat.

- Fewer animals in unethical environments.

- Theoretically, more control over the fat and nutrient content, as well as meat quality, of cultured meat versus traditional meat.

This all sounds pretty great. So how does this meat culturing work?

In short, you need muscle stem cells from an animal — maybe a cow, maybe a chicken, or maybe…a mouse?! Well, according to this document on cultured meat from Chalmers University of Technology in Sweden, mouse cells are “much easier” to work with (nothing is mentioned of the taste). These stem cells would need to be continuously bathed in nutrients and periodically stimulated to get “exercise” like normal muscles would. And unless they want all cultured meat to look like minced meat, researchers still have to find a way to simulate the blood vessels that feed normal muscle.

Muscle stem cells...yum!

To be fair, cultured meat is a fantastic concept with myriad implications for the environment and even world hunger. But for me and people like me, it may take a while for the psyche to warm up to the idea. As it turns out, though, there should be plenty of time before I have to make a call between traditional and cultured meat at the grocery store: cultured meat is currently expensive to produce and funding is limited for this type of research,  many of the culturing methods are only in the preliminary stages, and a whole lot of testing would need to be done before the meat could be brought to consumers.

On the flip side, some say that producing less traditional meat will only increase world hunger while failing to noticeably impact global warming, which is dominated by emissions from activities like transportation and electricity production. Farming smarter, not less, could be more feasible than trying to grow meat in vitro.

In any case, I imagine that the choice between traditional meat and cultured meat will be one that I’ll get to make in my lifetime. Maybe (hopefully?) I’ll be able to stomach the notion of meat that’s been grown in a lab by the time that day rolls around.

In the meantime, I’d love to get your thoughts on cultured meat – leave a comment!

(Pssst! The winner of the Try Nerdy merchandise giveaway will be announced Friday morning during the 8:00 hour – start Tweeting if you haven’t already!)

Tuomisto HL, & de Mattos MJ (2011). Environmental impacts of cultured meat production. Environmental science & technology, 45 (14), 6117-23 PMID: 21682287

Because many complications can occur with any type of transplant, one example being immune rejection, stimulating the body’s own stem cells to make new heart cells would be ideal. This idea serves as the motivation for this entry’s article.

Title: De novo cardiomyocytes from within the activated adult heart after injury

Authors: Nicola Smart, Sveva Bollini, Karina N. Dubé, Joaquim M. Vieira, Bin Zhou, Sean Davidson, Derek Yellon, Johannes Riegler, Anthony N. Price, Mark F. Lythgoe, William T. Pu & Paul R. Riley

Date of publication: June 8, 2011

Direct link: ttp://www.nature.com/nature/journal/v474/n7353/full/nature10188.html

PMID: 21654746

Abstract: Knowing that there are several limitations to cell transplantation as a means of replacing damaged heart tissue following a heart attack, these researchers set out to try to identify a pool of stem cells in the adult heart that could potentially be utilized to restore damaged heart tissue from within. The authors ultimately found that these adult stem/progenitor cells could be identified by the expression of a gene called Wt1, which was turned on after treating with a peptide (essentially a small version of protein) called thymosin b4. These progenitor cells are suggested to have derived from the epicardium, which is the outer layer of the heart. Stimulating these adult stem cells with thymosin b4 caused them to integrate with damaged heart tissue and become mature cardiomyoctyes (heart muscle cells). Developing a way to utilize these inherent progenitor cells to help mend a damaged heart would be a powerful way to minimize the use of drugs or the need for transplanted tissue.

Methods: The authors made use of mice whose cells would turn green if the Wt1 gene was turned on – recall, the hypothesis is that if Wt1 is turned on in a cell, then that cell may be a heart stem cell. The fact that the cells would turn green when the gene turned on allowed for easier studying of those particular cells later. Mice were injected for 7 days with thymosin b4, because it had previously been shown to improve the function of heart stem cells, before being induced to have a myocardial infarction (heart attack). The researchers induced heart attacks by anesthetizing the mice and then sealing off a major artery of the heart (the left anterior descending artery).  At 2, 4, 7, or 14 days after sealing the artery, the heart was removed and those green progenitor cells could be studied within the heart tissue or isolated from the tissue. Additionally, the authors used some of these isolated stem cells to transplant them into other mice that had had heart attacks, to see if the stem cells could improve the condition of the mice.

Results: Mice pretreated with thymosin b4 before myocardial infarction had significantly more progenitor-like cells in their hearts after myocardial infarction, compared to mice that did not receive these injections. Although mice injected with a negative control did show an increase in progenitor cells following a heart attack, thymosin b4 significantly increased this response. The authors could see that these cells had traveled to the scar on the heart caused by the heart attack, and had started to express some of the genes specific to heart cells – meaning that the stem cells were turning into heart tissue and helping to heal. The progenitor cells isolated from one mouse and transplanted into the heart region of another mouse that had had a heart attack started to turn into heart cells and help to heal the injury in the heart of the recipient mouse as well.

Bottom line: In mice, which are clearly not humans but are the most closely related common lab animal, these researchers identify a pool of cells in the heart with the ability to generate additional heart cells following a heart injury, and this ability is significantly enhanced by the peptide thymosin b4. Although thymosin b4 treatment was not as efficient as an ideal human cell-based therapy would be, the work in this article justifies the search for other molecules that can similarly increase the response of progenitor cells in our hearts to heal and replace the damaged heart tissue that results from heart attacks.

Interesting fact: Working with mice is expensive. Maintaining a mouse cage costs $1-2 per day. Just 30 mouse cages, which this work seemed like it would have needed, at least, would cost $10,950-$21,900 for one year of research. And it is typical for the research in a major publication to represent at least a year’s worth of work, if not four or more.

Stem cells: To make a human, or most any other animal, the first step is sperm meeting egg. The two cells fuse and since each one contains half the genetic information for a whole animal, the fused sperm and egg are considered one cell, called a “zygote.” Obviously an animal is ultimately made up of more than one cell, so the zygote needs to divide to become two cells, then four, then eight, then sixteen, and so on. From that one zygote, there needs to be created a heart, skin, lungs, bone – many kinds of tissues. To get from one cell to many different kinds of cells, many of the early embryonic cells are stem cells or have varying potencies to divide and produce other types of cells (“other types of cells” can include heart cells, fat cells, kidney cells, and even other stem cells). Even as an adult, some of our tissues retain a small population of stem cells so that in the event of injury, for example, damaged tissue can be remade.

 
Smart N, Bollini S, Dubé KN, Vieira JM, Zhou B, Davidson S, Yellon D, Riegler J, Price AN, Lythgoe MF, Pu WT, & Riley PR (2011). De novo cardiomyocytes from within the activated adult heart after injury. Nature, 474 (7353), 640-4 PMID: 21654746