Showing posts from February, 2011

Resistant Starch & Butyrate: Eades' Shmashthematics

While finally finishing off my last post on short chain "fatty" acids, I was reminded of a whopper of a post on Dr. Eades' blog that I came across a long ago on resistant starch and butyrate.  This post, too, has been in my Drafts for a very long time waiting for some finishing touches. I came across this whilst I was looking into soluble fiber, low carbing and stalling and discovered that for all intent and purposes, SCFA's are carbohydrates metabolically, not fats at all.  On LC forums I was repeatedly told or reading that soluble fiber is not really a carb because it is converted to a fat therefore doesn't stimulate insulin (I've got a fair amount of info on this to summarize in a future post).  So this was one of the first things I began inquiring after. I had read several highly informative pieces by Eades through links in discussions, etc.  But when I found and read this one, it perked my "fact check" bunny ears right on up.   He seem

Adipose Tissue Characteristics in Obese Teens & Insulin Resistance

Cellularity and Adipogenic Profile of the Abdominal Subcutaneous Adipose Tissue From Obese Adolescents: Association With Insulin Resistance and Hepatic Steatosis Yes ... I'm going to be on a bit of a bookmarking post spree here :-) This study looked at fat cell size and proliferation in obese teens and compared this to IR and fatty liver.  This study seems to be consistent with the whole "critical threshold" or "normal fat capacity" theories on why some obese are relatively "metabolically healthy" while others are not.  I've not, however, had a chance to read thoroughly. Conclusions:  A reduced lipo-/adipogenic capacity, fraction, and estimated number of large subcutaneous adipocytes may contribute to the abnormal distribution of abdominal fat and hepatic steatosis, as well as to insulin resistance in obese adolescents. Thinking out loud:  It seems more and more to me these days that abdominal fat - visceral in particular - is our short term bu

Subcutaneous and Visceral Adipose Tissue: Their Relation to the Metabolic Syndrome

Subcutaneous and Visceral Adipose Tissue: Their Relation to the Metabolic Syndrome Another bookmarking post of sorts. One interesting statement: ... in a review of 23 published studies of intervention strategies   to promote loss of visceral adipose tissue... ( 32 ) concluded that   individuals with greater visceral fat mass, either through an increase   in body weight or the propensity to store fat in the visceral depot,   lose more visceral fat when adjusted to the loss of body fat, regardless   of the intervention applied (caloric restriction, pharmacological   therapy, or exercise) because the visceral adipocyte has a higher   lipolytic rate also in the steady state.  For me, this makes my body fat distribution change all the more confusing, except that it does seem I'm talking more subQ belly fat than visceral in my case. 

Free Fatty Acids (FFA), A Link between Obesity and Insulin Resistance

FREE FATTY ACIDS (FFA), A LINK BETWEEN OBESITY AND INSULIN RESISTANCE Evidence, gained from human studies, is reviewed showing that elevation of plasma FFA levels produce peripheral and probably also hepatic insulin resistance in obese healthy and diabetic subjects. First, plasma FFA levels are elevated in most obese subjects. Second, physiological elevations of plasma FFA inhibit acutely as well as chronically insulin stimulated glucose uptake in a dose dependent fashion. Responsible for this inhibition is a FFA induced defect in insulin stimulated glucose transport and/or phosphorylation which develops after 3-4 hours of raising plasma FFA and a second defect, consisting of inhibition of glycogen synthase, the rate limiting enzyme of glycogen synthesis, which develops after 4-6 hours. FFA induced inhibition of fatty acid oxidation (Randle effect) does not affect insulin stimulated glucose uptake or glycogen synthesis and thus does not cause insulin resistance. Elevated plasma FFA

Free Fatty Acids/NEFA and Arrhythmia

From:   Circulating Nonesterified Fatty Acid Level as a Predictive Risk Factor for Sudden Death in the Population  In ischemic conditions, concentration of circulating   nonesterified fatty acids (NEFA) is increased and has a proarrhythmic   effect that is responsible for ventricular tachyarrhythmias.   In nonischemic patients, high NEFA plasma concentration has   been shown to be associated with frequent premature ventricular   complexes and increased familial risk of cardiovascular disease,   but its relation to sudden death has not been studied. We assessed   the role of circulating NEFA in sudden death in asymptomatic   men in a long-term cohort study. Above is the abstract for the study.  Something that might not be alarming to some.  The association could be due to a co-correlation with insulin resistance, for example.

Screen Time = Eat More?

Interesting study discussed by Yoni Freedhoff over at Weighty Matters Playing Video Games Makes You Eat More? The video game players used ~20 cal more but ate ~80 cal more than simply seated controls in a subsequent lunch.  That caloric excess was not compensated for by eating less later in the day.  Kind of a fascinating result!

Elevated Free Fatty Acids: Detrimental?

As many of my readers know, I've been challenged lately on my beliefs on NEFA.  So I thought I would summarize my thinking on this in a post rather than having several comments scattered amongst a few threads.   I'm not going to be referencing my post here at this time (it's too time consuming to do so at the moment).  If/when I have the opportunity to do so in the future, I'll do a bumped update.   These are my thoughts based on extensive research of the peer review literature on this topic, in almost all cases, considered review of full text articles including reading as many supporting citations in major reviews as possible.  Over the past year I have read at least a hundred such articles. Elevated non-esterified or free fatty acids (NEFA/FFA) are a symptom associated with insulin resistance, Metabolic Syndrome (aka Syndrome X) and Type II diabetes.  The overwhelming evidence in the literature points to elevated NEFA being more than just associated with these condi

Hypertension, Insulin and Free Fatty Acids (Part I)

Obesity Hypertension Is Related More to Insulin's Fatty Acid Than Glucose Action Although resistance to insulin-mediated glucose disposal has emerged as a link between abdominal obesity and hypertension, abnormalities of nonesterified fatty acid metabolism may play a greater role. ... Fatty acid concentration and turnover were markedly more resistant to suppression by insulin in obese hypertensive than in lean or obese normotensive individuals. ... The data indicate that blood pressure is related to the effects of insulin on fatty acid metabolism. The findings raise the possibility that resistance of hormone-sensitive lipase to insulin participates in elevating the blood pressure of abdominally obese hypertensive subjects by increasing fatty acid concentration and turnover. I'm C&P'ing the entire Introduction because it contains live links to background references some readers may be interested in.

Up for debate: Diabetes Mellitus or Diabetes Lipidus

In light of recent comments suggesting I'm barking up the wrong tree with my concerns over free fatty acids, I decided to bump this July 2010 post.  I think it is an excellent review.  The rest of the post remains unchanged. For Debate Diabetes: mellitus or lipidus? Introduction Since ancient times the search for causes of diabetes was related to the sweetness of urine and other body fluids. In England, Thomas Willis (1621–1675) was among the first to taste the urine of diabetic patients and declare that “its sweet taste was imbued with honey sugar” with the supposition that it was derived from blood. This finding led to the addition of “mellitus” to the word diabetes. We should reconsider whether the definition of diabetes as mellitus is justified. The traditional emphasis on the insulin-glucose axis with respect to examining glucose tolerance, although diagnostically useful does not explain the basic pathophysiological mechanisms operating in diabetes. The glucose-insulin axis

Don't be a Yo Yo! (Effect of weight change on energy expenditure)

Effects of experimental weight perturbation on skeletal muscle work efficiency, fuel utilization, and biochemistry in human subjects Or in plain English, what happens to your metabolism when you gain or lose weight. Maintenance of a body weight 10% above or below that “customary” for lean or obese individuals results in respective increases or decreases in the energy expended in low levels of physical activity (nonresting energy expenditure, NREE). These changes are greater than can be accounted for by the altered body weight or composition and are due mainly to altered skeletal muscle work efficiency at low levels of power generation.

Internetiquette II: Big Fat Head, etc.

Warning:  This post contains absolutely no science.  If you are looking for science, please look at 99% of the other content on the blog.  If you are offended by non-science posts on a predominantly science-based blog do not read this. Yes ... that means you, insert name here  , if after reading this anyway, you're compelled to comment on how and what I should write about here. 

Oh the Irony!


Failure of LC/HF Diets to Suppress NEFA Release

Thanks to reader MM, I have procured a full text copy of the following study that I've discussed a bit previously:   Lack of suppression of circulating free fatty acids and hypercholesterolemia during weight loss on a high-fat, low-carbohydrate diet A bullet pointed, sometimes paraphrased abstract/summary: This study compared a low carb (less than 20g/day, no fat content provided but "high fat") diet to a high carb diet (55% energy, 30% fat)  Fasting, 24 hour AUC (cumulative exposure) and time courses for metabolites were measured during weight loss. Subjects were healthy, obese adults (n = 32; 22 women, 10 men) - diabetics and those with a history of CVD were excluded. The study lasted six weeks.  A 24-h in-patient feeding study was performed at baseline and after 6 wk. Glucose, insulin, free fatty acids (FFAs), and triglycerides were measured hourly during meals, at regimented times. Remnant lipoprotein cholesterol was measured every 4 h. Results:

Non-esterified fatty acid metabolism and postprandial lipaemia

Non-esterified fatty acid metabolism and postprandial lipaemia Yet another gem from ... who else? ... Keith Frayn! Non-esterified fatty acids (NEFA, or free fatty acids) are an important metabolic fuel. Both the concentration of NEFA and their flux through the circulation vary widely from hour to hour, reflecting nutritional state and physical activity. Inappropriately elevated plasma NEFA concentrations may have a number of adverse effects on both carbohydrate and lipid metabolism. As my regular readers know well, this is a focus of my research. These adverse effects are likely to be most marked in the postprandial period, when NEFA release from adipose tissue is usually suppressed. Although the regulation of NEFA release in the postabsorptive state is well understood in molecular terms, the predominant pathway for release of NEFA in the postprandial state is the action of lipoprotein lipase (LPL) in adipose tissue capillaries on chylomicron-triacylglycerol (TG). Fatty acids released b

Internetiquette & The Full Email Exchange with Gary Taubes

Warning:  This post contains absolutely no science.  If you are looking for science, please look at 99% of the other content on the blog.  If you are offended by non-science posts on a predominantly science-based blog do not read this. UPDATE  2/9/11 ~1:30 EST:   I somehow chopped out the emails!  Have edited them in.  Thanks MM for the alert!

IDE (Insulin Degrading Enzyme): Insulin & Glucose

Glucose inhibits the insulin-induced activation of the insulin-degrading enzyme in HepG2 cells This was an in vitro study done with human liver cells (HepG2 cell line).  The cells were incubated with either a normal glucose solution (1g/L = 100 mg/dL common units for blood glucose) or a high glucose solution (4.5g/L = 450 mg/dL) and treated with insulin for 24 hours vs. untreated cells.  The activity of insulin degrading enzyme, IDE, was measured.  (For those not familiar with IDE, here's the Wikipedia entry on it) Here are the results for one insulin concentration studied: (as always you can click to enlarge) Note:  cytosol = fluid inside the cells So we see that at normal glucose levels insulin markedly stimulates IDE inside the cells while mildly suppressing it in the membrane.  The total effect is a marked stimulation of IDE by insulin.  This effect is almost nullified by hyperglycemia with an insignificant uptick in cytosolic activity and an uptick in membrane activity f

Question on Gastric Bypass Surgery

I'm not talking lap band here but the ones where you detach and reattach further down on the intestines like here . Does some sort of digestive tract flush/cleaning or fasting/cleansing like for a colonoscopy precede these procedures?   Thanks :-)

Free Fatty Acids & Sudden Cardiac Death

I finally found the paper I've been alluding to here for a while, but have some other things in the works both for this blog and in my "real life" so that I'll just do a bookmark for now.  Keith Frayn's Metabolic Regulation is just a gift that keeps on giving as in re-reading some parts that led to a blurb on FFA's citing one author of this review. Sudden cardiac death: the lost fatty acid hypothesis

More Todd Becker (Getting Stronger blog) on Insulin

I am really enjoying the back and forth that has ensued between Todd and I following my Insulin Wars installment on his commentary on James Krieger's series on insulin.  For those who are unfamiliar, here are the links to content on this blog: Insulin Wars IV: Todd Becker of Getting Stronger blog Insulin Wars IV.1: Todd Becker of Getting Stronger blog responds I received an email from Todd that he will be responding once again so stay tuned for version IV.2 and continued discussion!  Todd certainly gets the old gray matter working.  Reading a bit more at his blog I think we have some areas of agreement regarding this beleaguered hormone. In the meantime, Todd has posted a discussion of his own at his blog:   Does insulin make you fat?    I have some comments on that to add over there, hopefully soon.   Also, don't miss Todd's interview with Jimmy Moore .  I haven't listened to this one yet, but I will be!

Of Mice & (Wo)Men: When's the last time you saw an 5'4" 130 pound fat woman?

I'm always amused when a rodent study that seemingly counters the calorie-based theories on obesity comes down the pike.  In predictable fashion, someone in the LC webosphere will pick up on it and use it as an example to counter calorie-based theories on weight/obesity.   A recent example of this is brought to us by low carbers' favorite comedian edutainer, Tom Naughton:  Fat Mice & The Laws of Thermodynamics  that referenced the following study:   Mild calorie Restriction Induces Fat Accumulation in Female c57BL/6J Mice .   Now Tom starts out misrepresenting things by picturing a fat mouse, likely an ob/ob.  This study actually involved females of the strain pictured below: Kind of a cute little critter, no?   The study was also conducted in the context of calorie restriction and its demonstrated increase in longevity of mice.  They are not a mutant strain genetically predisposed to obesity.