Metabolic syndrome is just a descriptive term for a general sub optimally functioning endocrine system as concerned with glucose handling capability. I've read quite a bit on this over the years, and the whole subject is still being explored and understood, especially concerning leptin. Not just obese ectomorphs can be leptin or insulin resistant. Skinny endomorphs can to. There's plenty written about it. I didn't make it up.
I have kept detailed spreadsheet records of diet and experience/relations/conditions about myself for years. I'm not flying blind and self diagnosing willy nilly. I pay very careful attention to my body and reactions, and have been a competitive cyclist, and a climber and lifter for many years using all kinds of dietary combinations and noting performance and reactions.
And what does self diagnosing even mean? That I take responsibility for my body and pay attention to its signals? That I seek knowledge? That I choose not to accept that only doctors have the right to own and dispense medical knowledge or judgment, most of whom are in far less optimal physical condition that I keep myself in?
I digress. Insulin resistance at first makes one hyperglycemic. Then, as the muscles don't receive the glucose and the blood levels become high, the brain gets too much, and the rest gets stuffed into fat, resulting in hypoglycemia afterwards. It's a yo yo thing.
If I must, when I lift heavy or endurance train HARD AND LONG, my body absorbs sugar and carbs excellently with no adverse reactions. All other times I feel like shit and or am awakened in the middle of the night starving hungry if I screw around with carbs.
More digression. The point of this thread is to explore the possibility of clenbuterol causing insulin resistance and by what mechanisms, not about me or my so called self diagnosing.
I agree rat studies suck as people aren't rats. So I hope someone can offer some human based research. Diabetic trainees on other sites have all said when on clen they feel like shit and their blood sugar rockets, and they have to up their injected insulin greatly.
If my insulin/glucose regulatory systems are not so well functioning, this would make sense that I too felt like shit.
Btw I only took clen one day, five days ago. It has a half life of a few to several days depending on who you ask. After being free of night-starving-low-blood-sugar-wakings for some time due to diet being dialed in, clen caused it again with no change. I'm seeking the reason. Next night, clen still in my system, happened again. No change in diet at all. Then, last two nights, as clen cleared, slept like a baby. Diet is spot on with a gram scale on ever single item. No changes. Intermittent fasting leangins unchanged.
U have no idea what you're talking about, no offense. Did you even bother to check my other posts or look into anything I stated. I have spoken about MetS in the past on this forum. I'm not trying 2 b rude & ugly, but its ppl like you on this forum that make me wonder sometimes y I even bother 2 attempt 2 assist ppl on here. Reading AND Understanding what you're reading r 2 entirely different things. For example, I'm sure many ppl have read classical literature like Hamlet & The Brothers Karamazov, but all those ppl didn't understand what they were reading, at least not to the fullest extent. So, either you are not understanding what you are reading, or reading the wrong information in general.
First, your definition of MetS isn't correct. The general definition of MetS is: A cluster of health related disorders & risk factors that significantly increase the risk of CVD & T2DM. Reputable organizations that study & research MetS will have their own specific definitions based upon that. For example, the IDF definition is in this link:
IDF Worldwide Definition of the Metabolic Syndrome | International Diabetes Federation
Also, for proper diagnosis of MetS, you have to have a certain # of these health disorders/factors. Some organizations state that some of these disorders are mandatory for MetS to be present. For example, the IDF I previously mentioned stated that Central Obesity needs to be present to have MetS (
http://www.idf.org/webdata/docs/MetS_def_update2006.pdf). Other organizations feel that Insulin Resistance has to be present. You haven't been diagnosed w/ either, so you don't have MetS. Have you ever had a FPG or OGTT? I'm sure you know sum1 who is diabetic, so just request to use their BG meter & check it in the morning after sleeping well & an 8-12hr fast. I'm sure it will be under 100, hell w/ how active you state you are, prolly even in the 80s range. U attempting to talk about BOTH insulin resistance & leptin resistance is just foolish, when udk the diagnostic criteria for MetS to begin with.
Also, your pathophysiology of insulin resistance (IR) is way off & even laughable at times. Idk where you're getting this "hypoglycemia" information + you need to state how severe the IR is you are attempting to describe. When ppl first get IR, it is speculated to occur first in the muscles (muscles or liver actually, just depends who you ask), so you actually are correct in this regard. However, the glucose that is supposed to be used to replenish glycogen stores in the muscle in these types of ppl is actually diverted back to the liver for de novo lipogenesis (DNL), resulting in fatty liver & atherogenic dyslipidemia. Here, read this from the abstract I pulled provided here (
The role of muscle insulin resistance in the p... [Annu Rev Nutr. 2010] - PubMed - NCBI) that states this (+ I strongly suggest you read the whole review 2 bring you up 2 speed on what I'm talking about): "We review the potential primary role of skeletal muscle insulin resistance in the pathophysiology of the metabolic syndrome, showing that in lean, young, insulin-resistant individuals, impaired muscle glucose transport and glycogen synthesis redirect energy derived from carbohydrate into hepatic de novo lipogenesis, promoting the development of atherogenic dyslipidemia and NAFLD."
For the fact that the "brain uses too much" made me literally LOL. Idk where you read that, but glucose concentrations/levels & energy needed for the brain to function is regulated well (http://www.jneurosci.org/content/29/21/7015.full (Relationship among Brain and Blood Glucose Levels and Spontaneous and Glucoprivic Feeding)). If the brain gets 2 much glucose, it is actually toxic, as observed here in a chronic, hyperglycemic state:
Brain glucose levels are elevated in chronically ... [Metabolism. 2002] - PubMed - NCBI
A diabetic brain isn't hypermetabolic, where it needs more glucose & DNL in the brain is neglible. I mean, c'mon, if high DNL activity in the brain where possible, think of the CONSEQUENCES of that, so your statement here of, "brain uses too much" is just silly.
But, back to the point of how you feel ur IR. I find this very hard to believe w/ how active you are. Read this study that shows how young, IR ppl reversed their IR after just ONE BOUT of endurance training:
Reversal of muscle insulin resistan... [Proc Natl Acad Sci U S A. 2011] - PubMed - NCBI
Which shows how you self-diagnosing yourself as having MetS & IR is complete non-sense. It is also a, "smack-in-the-face" for physicians who have been properly trained to diagnose ppl based on tests & judgment. I'm sure Drs. Scally & Jim on this forum will tell you the same.
Back to IR though, as I just spoke of ppl that begin to have IR, which is speculation in the muscle first. However, if ppl begin to have IR in the other muscle glucose responsive tissues (liver & fat), you can start to store fat in other places, such as the liver, kidney, muscle, even heart, which is called ectopic fat. I recommend you google, "lipotoxicity and ectopic fat" for more info. So, in this case, when the fat becomes IR, even it cannot use the extra glucose for DNL properly, so you are wrong in this regard as well. As for animal studies, they are really good b/c you can control so many factors not possible in pertinence to human studies. Lastly, hunger & fatigue can be the result of literally 1000s of different things, so pinpointing it as having MetS/IR is comical, especially considering how active you are. I felt my general answer about clen was a suitable enough answer, I just needed to "get you back on course" w/ everything else, which is y the post is so long.
This paper will keep you very busy in terms of bringing you up to speed on IR, T2DM, & glucose homeostasis (
http://diabetes.diabetesjournals.org/content/58/4/773.full.pdf). As for MetS, just please look for reputable info from good organizations such as IDF, WHO, AHA, etc.). I have plenty of other information I can email you if you have problems obtaining papers, as I can send you the pdfs if you prefer. Just let me know, take care.
I've read other posts you have in this thread, so I'm gona talk bout them along with this 1 I've place in my post. I think you got some things backwards, if ur an ectomorph, than Idk y ur saying you have metabolic syndrome, as a core condition of MetS is central obesity. Do you have that, or are you self-diagnosing yourself like you are with the insulin resistance thing. IR will have cause HYPERglycemia & NOT hypoglycemia. Glucose intolerance testing (e.g. FPG, OGTT) will attempt to test for IR, but its actually difficult to test for clinically. Have you ever even checked your BG b4? Do you have (atherogenic) dyslipidemia and/or hypertension? These are other core components associated w/ MetS, which I highly doubt you have.
