Marc Interviews Nicole Rogers

Posted: April 20, 2010 in Interviews, Lifestyle, Nutrition, Training

First off, my apologies as I’m breaking blog-etiquitte (again) by posting a long article. But I wanted to run this anyway, as it’s one of my favorite interviews. Also, this interview was done two years ago, so some minor things have changed. Anyway, Nicole is a great girl with a ton of interesting things to say, so pop some adderall and dig in.

Nicole has a B.S. in Exercise Science, a Masters in Cell and Molecular Nutrition, and a PhD in Biochemistry and Molecular Nutrition. You can find her name tacked on to quite a bit of published research as well as some various well respected texts.

Academics aside, she’s right in the heart of the physique game and has some compelling things to say. We’re hitting all of the hot topics of scientific physique enhancement and Nicole has brought some exciting information to the table. This is one interview you want to pay attention to.

So give us a day in the life of Nicole Rogers. A brief rundown of the ins and outs, if you would.

Sure.  I wake up around 6:30 am and head immediately to the gym down the street.  Then it’s home to pick up my dog and walk her around Beacon Hill or let her run along the Charles River.

Finally it is off to the lab around 9:30 am, and once I get there everyday is unique, which is part of what I love about it.  An average day consists of experiments, research, writing and attending various seminars and meetings.  I usually leave the lab around 7:30 pm and then meet with clients if necessary, take my dog to the park, and/or head back to the gym for cardio.  I try to get to bed by 11 pm.

Wow, long day at the lab. Also more ammo for people that say they don’t have time to train. Suck it up, fatties.

You’ve spent some time on stage, talk a little about your competitive history, overall take from it, would you do it again, etc.

My first fitness competition was in the summer of ‘03 in Denver, where I won the Colorado State Fitness Championships. The following year, after moving to Boston, I won the Bev Francis Atlantic States in NYC. My final show to date was in Vegas for the 2004 USA Championships, where I placed 5th.

The other four were obviously nailing the judges.  As a whole, was your overall experience with competing positive?

Competing was a wonderful experience! It was so fun to see what level you can take your body to when you really put your mind to it. There are some things that are best learned first hand, and that experience taught me so much about myself as well as training and nutrition in general.

As far as competing again, I would love to, especially after being recently diagnosed with diabetes. I feel like it would be a whole new challenge and that I would again learn so much. But it won’t be for a while. My time constraints and career goals just won’t allow for it at this point.

Glad to hear it, your conditioning was amazing at your previous shows and it would be great to see you on stage again.

I want to get more into the diabetes thing in a bit, but first discuss your current training, and how it varies throughout the year.

I have spent the last 3 months trying to replace some of the muscle that I lost through my diagnosis last year. It’s amazing how quickly lean mass disappears in the absence of insulin!!

Something to think about…

Starting about a month ago, I’ve shifted my focus to leaning out for summer. To do this (and this has worked tremendously well for me previously) I weight train 4 days on / one day off, and split the muscles into a 3-day split. But I have 6 different workouts: the first 3 days I hit the muscles with higher intensity and some power movements. These workouts are really built around the core exercises such as bench press, squats, deadlifts, etc, performing high sets and low reps for each movement.

The next 3 workouts I do higher volume and less rest. I start with some of the core exercises here as well, but just a couple sets and then bring in a lot more variety in the types of exercises, reps, and tempos that I choose (Mechanical Advantage Drop Sets, 1 + 1/3’s, etc). I like to use these workouts to incorporate some fun fitness specific exercises, such as one-arm push-ups, walking on my hands, press handstands, burpees, etc, especially when I’m prepping for a show. (See article HERE for some Mechanical Advantage Drop Set ideas)

As for cardio, I do 10-15 minutes of high intensity interval training (HIIT) post-lifting after 3 of those 6 workouts. I try to do 30-45 min of a more steady state cardio at night 2-3x per week when I get the chance.

Love it, sounds like a great setup.

Discuss your current nutrition a little, and how does this change when you’re not prepping for three months of bikini-induced heart breaking?

My nutrition definitely changes a bit throughout the year, primarily through the avenue of carbohydrate manipulation…more when I am trying to gain muscle, and less when I am leaning out. This seems to work really well for me. But of course, this last year has been really quite unique as I’ve tried to get a handle on my diabetes.

I bet…and in a minute we’ll get all over that diabetes talk like black on Samuel L. Jackson. Any significant changes to protein and fat intake throughout the year, or type of carbohydrate?

My fat intake is always between 25-35%.  When my carbs are higher during muscle building phases I keep my fat intake at the lower end of the window, around 25%. As I decrease carb intake to lean out, I elevate protein intake just slightly, but I mostly substitute fat (increased to 35%).

So you’re more of a macronutrient manipulator than a calorie manipulator?

For the most part, with a few exceptions including periodic carb-up days and the last few weeks of a competition lean-out when I gradually drop calories (though never under 1200 kcal per day).

Check. What about those under your guidance, how many clients do you work with, in person and correspondence?

This past year I have really cut back in order to fully focus on finishing up my PhD. I am no longer training through a gym, so I mostly do fitness consulting (designing nutrition and workout plans).  As such, clients are more transient. I still work more regularly with quite a few fitness/figure/bodybuilding competitors though.

Anyone you’d like to mention that we should look for? Do you work with male clients, or mostly/all female?

I work with both males and females, although the majority of my clientele tends to be female. And one to keep your eye out for is Dr. Angel Allison. She is currently preparing for the USA Figure Championships in July and is looking awesome!

We’ll keep an eye out.

Moving on to your ever-nearing PhD completion…what is the area of focus, and what are your plans after completion?

I work in an energy metabolism laboratory, where we primarily study obesity and diabetes. I definitely want to continue diabetes and/or obesity research.  Upon graduation later this year, I will be seeking a post-doctoral fellowship at a pharmaceutical company. I love doing research and really want to be at the heart of the drug discovery process.

I make a great candidate for self experimentation with unknown and potentially dangerous pharmaceuticals. Just throwing that out there.

Let’s get into the dirty, sexy world of physiology. I want the inside scoop. You be Zoolander and I’ll be the sexy reporter Matilda…take me on a tour of the underground, behind-closed-doors world of late night runway Walk-Offs.

For starters, tell us any new interesting info you’ve come across about mTOR.

Well, mTOR is certainly a hot topic.  It seems like everyday there is something new coming out! And things just keep getting more and more complicated. It seems that now mTOR can help drive mitochondrial biogenesis (make more mitochondria) and increase the oxidative capacity of mitochondria. This means more fat burning potential!

Wow, that is news. Increased mitochondrial density is on my list of “things to get”. Very cool.

Something I’ve been looking into recently that strikes me as a potential player in the physique game is mVps34, tell us what you know about that.

Well I can’t say I know that much, but it will be very interesting to see if the human studies support some of the new animal data.  So it seems that mVps34, which is very abundant in skeletal muscle, may be a key player in regulating muscle protein turnover following resistance exercise.

You had me at “well”.

Keep it coming.

So basically, sitting upstream of mTOR, this lipid kinase allows mTOR to respond to intracellular nutrient status, namely amino acid depletion.

As such, mVps34 is inhibited by amino acid starvation, and additionally inhibited by AMPK.  It (mVps34) initially goes up about 3 hours after resistance training and stays up for quite awhile.

I think the working hypothesis is that depletion of intracellular amino acid pools (as would occur with exercise), activate mVps34 and promote autophagy in an effort to replenish amino acid pools and maintain mTOR activation to drive protein synthesis.

One last interesting tidbit is that its expression is higher in type I oxidative muscles…it will be interesting to see if there are any ramifications for this, and I for one am curious to find out if there are any gender differences in this protein. Time will tell.

It’s hard to deny that we are in the midst of an exciting time in the history of physiology; so many things are hovering on impending elucidation that those before us couldn’t have dreamed of comprehending.

As I wipe my tears away, let’s talk AMPK now that you’ve mentioned it. Any thoughts on the implications of its hypertrophy limiting capabilities, and the severity of impact of things like stimulants, ALCAR, etc. taken around workouts?

Well I don’t think this is actually an AMPK issue because I am not sure that stimulants taken around a workout will alter exercise-induced AMPK activity. Caffeine doesn’t.  What happens at rest and what happens during a workout are not necessarily comparable. AMPK is a cellular energy sensor, and as such it gets activated during exercise because ATP is being depleted.  I suspect that being such a tightly regulated energy sensor, nutrition is really going to be superior to any supplemental agent in terms of modulating its activity during exercise. (Chronic AMPK activation (i.e. pharmaceuticals) and inhibition of hypertrophy is another issue).

Indeed, it seems that AMPK activity may be tightly linked to glycogen storage. I just got back from a meeting where I heard this from Dr. Graham Hardie himself, a pioneer researcher in the AMPK field.   Interestingly, skeletal muscle AMPK activity (even during exercise) is inhibited by high glycogen levels.  Molecularly, the Hardie hypothesis is that a lot of cellular AMPK is actually bound to large glycogen molecules. Basically, under conditions where muscle glycogen levels are high, AMPK is more-or-less sequestered by glycogen and only able to phosphorylate glycogen synthase (GS, thereby inhibiting glycogen synthesis).

Interesting. As you continue upon this enlightening path, touch on the implication of those that sip on a carb/protein shake during workouts and its direct impact on AMPK.

So with high glycogen levels, only non-bound AMPK can phosphorylate its other well-known targets.  Thus, in a sequestering sort of way, glycogen inhibits traditional AMPK activity.  When glycogen starts to be broken down, as occurs with exercise, more AMPK becomes non-bound and is free to act on other targets, such as those in pathways leading to increased glucose uptake and fatty acid oxidation. This leads to the suspicion that sipping on carbs before and/or during a workout could decrease AMPK activity during workouts or perhaps prevent any increases that may occur with a supplemental agent that actually activates AMPK. But the jury is still out on implications of this inhibition. J

Very cool. Research tosses back and forth about peri-workout carbs, and this seems to throw the spotlight into a potentially significant, darkened corner.

Continue on a bit about the cage match between AMPK and hypertrophy.

Well, the concern on AMPK and hypertrophy is that AMPK inhibits mTOR.  But during exercise, AMPK gets activated as ATP gets depleted, (and yes, mTOR activity is suppressed), but this allows glucose to be taken up more readily, and fat to be oxidized at a greater rate. Good things when you are working out!

Ahh yes. This is where the interpretation/application of some of the current AMPK research has bothered me. Replication during actual exercise conditions is limited. Upstream inhibition by a lab technician needs to be scrutinized instead of embraced.

Exactly, it’s really what happens after exercise that matters in terms of hypertrophy. Post work-out AMPK activity declines as mTOR and mVps34 activity go up. Assuming proper nutrition follows training, insulin and amino acids will activate anabolic pathways.  And you may have better workouts with some caffeine!

Now if you are concerned about potential attenuation of insulin signaling with caffeine ingestion, well…a study hot off the press is demonstrating that co-ingestion of caffeine with PWO carbs actually increases glycogen re-synthesis. It seems that insulin-sensitizing exercise can override the insulin sensitivity impairments seen with caffeine ingestion in individuals at rest, at least in terms of glycogen re-synthesis.

But again, this actually doesn’t have anything to do with AMPK because caffeine did not increase AMPK activity that occurred with exercise, nor did caffeine prevent the decrease in AMPK activity that occurred with carb ingestion following the exercise. And furthermore, Akt phosphorylation was slightly higher after PWO carb ingestion in the caffeine group suggesting that maybe this caffeine benefit could spill over to other anabolic pathways (i.e. mTOR) as well.

If this is the same study I’m thinking of, it dealt with cycling, and the subjects were previously on low carb diets. Now, this is potentially huge research, and being a stimulant junkie I’m hoping this applies to a larger spectrum of subjects as much as the next guy…but give me your thoughts on application of this research to an audience of weight training individuals on varying carb diets. Potentially similar? I know this is theoretical, but throw us an opinion and we won’t hold it against you.

I agree with your point that I am extrapolating a bit, but I definitely think it’s similar and potentially relevant to weight training. For one thing, yes these were carb depleted trained men, but that only makes it more interesting that caffeine still had effects, as glycogen replenishing conditions were already more optimal, hence making it more difficult to see further benefit.

Great point, I hadn’t thought of it that way.

Clearly, the mechanism of this interaction between caffeine and exercise needs to be delineated. But if the mechanism is glycogen depletion, which is possible, then similar results could be predicted with weight training as well.  But of course cardio and weight training produce distinct hormonal milieu, and so clearly more studies will need to be done to confirm these data in different populations and different physiological states, but in the mean time, I for one will continue to caffeinate my cardio and weight training.

As will I, Miss Rogers.

Continuing down the path of underground physiology dirt, I don’t hear much about perilipin other than from you…give us a quick rundown and what it means to our health and undying quest for a super-sexy physique.

Think of perilipin as the gatekeeper of stored triglyceride.

I’m guessing that got your attention…

I’d say. Especially if said gatekeeper takes bribes.

Well I am actually not sure what this lipid droplet protein means to physique-enhancement in a lean individual, but molecularly, perilipin acts as a barrier to prevent lipolysis in the basal state, but enhances lipolysis in the presence of stimulation such as that occurring with catecholamines.

Upon catecholamine stimulation, perlilpin targets HSL (Hormone Sensitive Lipase) to the lipid droplet, thereby allowing triglyceride to be released and hydrolyzed. Interestingly, obese women have less perilipin and higher rates of lipolysis (obviously lipolysis does not equal fat oxidation!!).

That last sentence just made you a lot of friends around here…definitely a concept many people fail to realize and or accept. Really interesting link between catecholamines and HSL…do continue.

When we look to the mice, the perilipin knockout mouse is lean and resistant to diet induced obesity, seemingly a good thing, right? Well, these mice become insulin resistant with time, probably due to the high concentration of free fatty acids floating around.

Furthermore, TNFα (an inflammatory cytokine that promotes insulin resistance) decreases perilipin, thereby chronically increasing adipocyte lipolysis.  This is not a good thing and interestingly, a recent study showed that metformin (a popular drug used to treat type 2 diabetes) prevents this decrease in perilipin seen with TNFα treatment, at least in cells.

Finally, I know of one obscure paper that showed that a plant extract could decrease body weight in females in part by decreasing perilipin, but I am still skeptical. I’ll leave you with this…there are currently some really interesting studies being done to look at gene-diet interactions with relation to perilipin. We’ll have to wait and see I guess!

Great stuff there Nikki, something to keep an eye on. And another good reason to have you developing pharmaceuticals…

Lets get into estrogen…give us a rundown of receptor subtypes, some common misconceptions, and any other inside info you have.

Well, as some background, there are 2 well characterized nuclear estrogen receptors: ERα and ERβ. These function as classic nuclear steroid receptors by binding to response elements in target genes and ultimately altering transcription (genomic effects). But these receptors can also move to the plasma membrane and activate signaling cascades upon ligand binding (non-genomic rapid effects). Furthermore, there is some suggestion that a newly described g-protein coupled receptor (gpr30) also binds estrogen, again initiating signaling cascades.

So we’ve got ERalpha and ERbeta activity coming from multiple angles, as well as a non estrogen receptor responding to estrogen. Check.

Right. I guess the major misconception is that estrogen is all bad, because it is actually quite protective, at least in terms of preventing metabolic pathology.  One of the things that estrogen does in humans is promote subcutaneous fat storage (versus the bad stuff – visceral), particularly butt and leg fat. While this isn’t necessarily good for physique-enhancement, it is actually the safest place to store body fat and is probably the reason that females are protected from metabolic disease compared to men.

Very important point in gender based fat distribution.

Yes, and not only adipose tissue my friend…but my thesis work is actually aiming to get a better understanding of estrogen’s role in skeletal muscle physiology, a surprisingly understudied area.

We have found that estrogen increases LPL in muscle, while decreasing it in fat tissue. This results in a partitioning of fatty acids away from adipocytes and towards skeletal muscle where these FFA’s are likely oxidized.  In support of this, we also saw that estrogen increased muscle PPARδ expression (a master regulator of fat oxidation). Furthermore, we found that estrogen and a metabolite of estrogen (2-hydroxyestradiol) can rapidly activate AMPK in muscle, another mechanism for increasing fat oxidation, as well as Akt, an important signaling molecule in the insulin cascade.

Based on that last sentence, I’m going to briefly interject on behalf of AMPK for an extremely brief and incomplete rundown of what it does…just to make sure we’re not losing anybody.

Think of AMPK as a fuel sensor in the cell, when stored energy is low; AMPK is activated to solve this problem. Above we mentioned that AMPK can be hypertrophy hampering, but that’s not the whole story. It also acts as a signal to activate pathways of increasing available ATP, such as fatty acid oxidation, which is a good thing.

Back to Nikki, and estrogen receptors…

So, estrogen receptors are clearly expressed in skeletal muscle, and there are obvious gender differences in terms of muscle quality and quantity.  Now clearly testosterone plays a role here, and probably progesterone as well, but estrogen is quite important too.

Skeletal muscle expression of estrogen receptors is something many people don’t realize. Generally speaking total skeletal muscle is obviously higher in males, but what about percentage of estrogen receptors in the skeletal muscle/relative expression…gender differences?

Well, for one thing, expression of ERs in muscle is way less than say uterine tissue. Now, from the limited studies that have been done to look at ERs in muscle, there actually don’t seem to be major differences between the genders. Males definitely express estrogen receptors, and estrogen is important to male physiology in that males with rare genetic estrogen deficiencies (aromatase or ERa deficiency) have profound glucose and lipid metabolism impairments and are quite insulin resistant. Interestingly, endurance trained males have higher muscle expression of both ERα and ERβ, probably due to higher type I fiber percentage. (Muscle expression of both receptors is higher in type I oxidative fibers.) But the relative expression and importance of ERα and ERβ in muscle is still quite unclear.

Really good info there. What about gender differences in adipose ER expression?

In terms of adipose tissue, it has been shown that female ERa expression is higher than ERβ in omental fat, but ERβ expression is higher than ERa in subcutaneous depots. And women with higher ERβ expression in omental fat tend to have greater adiposity. Just a correlation of course, but it’s possible that ERβ opposes ERa in adipose tissue.

Goes along with previous knowledge of visceral vs. subcutaneous fat often behaving in opposition.

Right! And actually the newest line of thinking is not so much that visceral is bad (again, metabolically speaking), but that subcutaneous is actually good! But that is a whole different story….So getting back to muscle, one of things that estrogen has been shown to do in rodents is activate myogenic satellite cells in response to muscle damage, thereby facilitating muscle recovery from exercise. Interesting! Now a lot of my work is not yet published, so I can’t say too much. But have no doubt; ovarian hormones likely have significant effects on skeletal muscle!

Interesting indeed. I just finished reading the full text of a new study about satellite cell activation and its role in hypertrophy, and zero mention of estrogen’s role. Looking forward to your inside info when your research is published. Is the role of estrogen in SC activation likely to transfer to humans, based on what you know?


You’re spittin’ gold here Rogers. I think we all have a new outlook on Estrogen after that compelling info.

Let’s talk a little bit about your Diabeeetis. Originally you thought you had a mid-road diagnosis if I’m not mistaken…as in not a pure Type 1 or Type 2. Explain that, and what you’ve learned through trying to manage insulin therapy while keeping a rockin physique.

When we initially discussed this some time ago, my diagnosis was incorrectly determined to be Type 2.  This after I showed up at the doc’s office having had blood sugar over 600 mg/dl (as high as a glucometer can read) for at least 8 hours. After going home with Metformin and no referral to an endocrinologist, I took it upon myself to seek a 2nd opinion and an immediate shot of insulin.

Thankfully I did, as it turns out I’m actually a true Type 1, meaning auto-antibody positive and no insulin production, and now I have a great doc to refer people I don’t like.

But back to the now, it’s been CRAZY having diabetes! With all of my knowledge, it’s still been a daily struggle to keep my blood sugar in check. I have a whole new respect for the pancreas, that’s for sure! Regardless, I’ve really tried to focus on it as a learning experience, which it TOTALLY has been.  My biggest battle came this spring when I started my attempt to get super lean for summer.  To my surprise and remarkable frustration, the body fat just wasn’t melting off as it has every year prior when I would stick to a clean nutrition plan (notably pre-insulin therapy).

As frustrating as this has been, it has ended up being somewhat serendipitous in that I have come to discover my new favorite hormone – a hormone that I sadly knew very little about prior to my diabetic struggles. It turns out that the pancreatic ß-cell makes 2 hormones. That’s right…not just the well appreciated insulin, but also the much lesser talked about cousin of insulin called amylin!


Basically, amylin is co-secreted with insulin acting to ultimately help control glycemia post-prandially.  It does this in 3 ways:

1) Slowing gastric emptying

2) Inhibiting gluconeogenesis

3) Sending the brain signals of satiety.

Well, us type 1’s who don’t have beta cells also don’t produce amylin. The result of this is high post-prandial glucose spikes and increased fat storage.

Let me explain my theory on the fat storage phenomenon…normal people produce insulin in the pancreas, which directly feeds the liver, so the liver actually sees more insulin than the periphery and gets a clear signal to shut down glucose production (release of stored glucose). My insulin however, now gets to the periphery from my subcutaneous injection site. Therefore my liver gets less insulin than necessary to completely inhibit gluconeogenesis (I would be severely hypoglycemic if I tried to give enough insulin to completely shut down hepatic glucose production). The end result is that I have to give MORE insulin to overcome the hepatic production and maintain euglycemia and “tight control” of my diabetes.

Now, lipogenic pathways are notorious for being super-sensitive to insulin (hence why severely insulin resistant individuals can still put on the fat!), so in the face of all the insulin I have been pumping to maintain euglycemia, it is actually no wonder that getting super lean has been tougher for me this year!

In terms of my diabetes control, obviously a huge concern, my A1c is still not optimal despite normal glucose readings pre and 2hrs post eating. I suspect this is because of high post-prandial glucose spikes. Normal people don’t go above 120 mg/dl, but I soar up past 200 mg/dl every carb meal!

Good thing I dose some antioxidants… Well now for the good news… a few weeks ago I started injecting symlin (an amylin analogue) with meals. It’s only been a couple weeks, but WOW! My glycemic control is amazingly better! I bet my A1c is plummeting as we speak!  It will take some more time to assimilate my fat loss data, but I am optimistic. I almost feel like normal person again! FYI, yo-yoing glucose levels over a range of 250 mg/dl throughout the day is NOT fun!

Really exciting stuff there. What a great discovery for you with regards to physique control as well as general well being.

I’m assuming that for a non-diabetic, injectable Symlin wouldn’t have a physique altering effect?

That’s a great question, but I don’t know the answer. It’s actually possible because I suspect amylin would suppress appetite in lean people too. I don’t know of any studies done yet in non-diabetic lean individuals, but I know they have given it to non-diabetic obese individuals and seen significant weight loss. It may eventually be approved as an obesity treatment, possibly in conjunction with other neuro-modulators.

More great info…I’ll be keeping an eye on that drug.

One last thing, then I’m sending everyone home to review their notes. During your masters you researched the effects of cinnamon on insulin sensitivity; can you give a brief overview of your findings?

I was doing in vitro studies with fat cells and muscle cells to try to reproduce some data showing that cinnamon increases insulin sensitivity.

Cinnamon had been shown to inhibit a phosphatase that de-activates the insulin receptor, and possibly even bind to the insulin receptor itself.  We never really got convincing data. Human studies have been conflicting, some showing beneficial effects of the spice, and others not reporting much going on. I suspect that cinnamon does some good things, but it depends on the extract, and the effects are small so you’d need a lot of cinnamon!

Righty oh…might want to hold off on the cinnamon until research is more suggestive towards a positive effect.

On that note, it’s time for the wrap up.

Huge thanks for an incredible interview; you really brought forth some great info. Hopefully we’ll be hearing more from you soon.

My pleasure, thanks for digging me out of the lab to share some knowledge!

Nicole’s Published Research:


D’Eon TM, Rogers NH, Stancheva ZS, Greenberg AS. Estradiol and the Estradiol Metabolite, 2-Hydroxyestradiol Activate AMP-Activated Protein Kinase in C2C12 Myotubes. Obesity 2008, in press (Epub April 10, 2008).

Rogers NH, Obin MS, and Greenberg AS.  Chapter 4: Obesity and Adipokines.  In Contemporary Endocrinology: Treatment of the Obese Patient. Editors: Kushner R and Bessenden DH, p69-85, 2007 Humana Press Inc, Totowa, NJ

Souza SC, Chrisofolette MA, Ribeiro MO, Miyoshi H, Strissel KJ, Stancheva Z, Rogers NH, D’Eon TM, Perfield JW, Imachi H, Obin M, Bianco AC, Greenberg AS.  Perilipin regulates the thermogenic actions of norepinepherine in brown adipose tissue. J Lipid Research, June 2007; 48(6):1273-9.


Rogers NH, Perfield II JW, Strissel KJ, Obin MS, Greenberg AS. Ovariectomy in mature mice does not increase food intake, but increases adiposity and adipose tissue inflammation. To be presented at NAASO 2008.

Rogers NH, Perfield II JW, Strissel KJ, Obin MS, Witczak CA, Goodyear LJ, Greenberg AS. Chronic estrogen deficiency in mice alters FoxO1 signaling in a mixed fiber skeletal muscle. To be presented at ENDO 2008.

Rogers NH, Witczak CA, Goodyear LJ, Greenberg AS. Estrogen rapidly phosphorylates AMPK, Akt, and AS160 in isolated rat soleus muscles. Experimental Biology, 2008.


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