The Carb-Sane Asylum

Response of plasma ASP to a prolonged fast  - Abstract only unfortunately OBJECTIVE:   To determine the changes in the plasma level of acylation stimulating protein (ASP) during a one month total fast in female subjects with marked obesity. DESIGN:   Patients with marked obesity underwent a month total fast, before, during (2 weeks), and at the end of which, a variety of relevant metabolic parameters were measured. SETTING:   A metabolic unit of a teaching hospital. SUBJECTS:   10 women with marked obesity were studied and the results compared with those in 16 age-matched controls. MAIN OUTCOME MEASURES:   Plasma ASP, lipoprotein lipids, apoB, free fatty acid, and ketone levels. RESULTS:   At baseline, fasting levels of ASP in the obese group were double that in control subjects (116 +/- 26 vs 53 +/- 30 nM P < 0.001). During the fast, ASP levels dropped progressively and were within the normal range at the end of the study (63 +/- 16 vs 53 +...

Subdivisions of subcutaneous abdominal adipose tissue and insulin resistance This is a very interesting article.  They looked at not only visceral vs. subQ abdominal fat, but differentiated between two types of abdominal SCAT (subcutaneous adipose tissue):  superficial vs. deep. There is a well described fascial plane within the SAT of the abdomen (18, 28), with the superficial adipose layer possessing compact fascial septa (Camper’s fascia), whereas the deeper layer of adipose tissue has more loosely organized fascial septa (Scarpa’s fascia).  Fat lobules of the two sites also differ. The superficial layer is characterized by small tightly packed lobules, whereas those of the deeper layer are larger and distributed in an irregular manner (28). The thickness of the deep layer appears more variable among individuals and especially in relation to obesity (3). The presence of these fascial planes and differences in histol...

Comparative toxicity of fatty acids on a macrophage cell line (J774) In the present study, the cytotoxicity of palmitic, stearic, oleic, linoleic, arachidonic, docosahexaenoic and eicosapentaenoic acids on a macrophage cell line (J774) was investigated. The induction of toxicity was investigated by changes in cell size, granularity, membrane integrity, DNA fragmentation and phosphatidylserine externalization by using flow cytometry. Fluorescence microscopy was used to determine the type of cell death (Acridine Orange/ethidium bromide assay). The possible mechanisms involved were examined by measuring mitochondrial depolarization, lipid accumulation and PPARγ (peroxisome-proliferator-activated receptor γ ) activation. The results demonstrate that fatty acids induce apoptosis and necrosis of J774 cells. At high concentrations, fatty acids cause macrophage death mainly by necrosis. The cytotoxicity of the fatty acids was not strictly related ...

Some more articles presented without comment for book-marking purposes: The anti-inflammatory and potential anti-atherogenic effect of insulin: a new paradigm Intensive Insulin Therapy Exerts Antiinflammatory Effects in Critically Ill Patients and Counteracts the Adverse Effect of Low Mannose-Binding Lectin Levels Anti-Inflammatory and Profibrinolytic Effect of Insulin in Acute ST-Segment–Elevation Myocardial Infarction

Is insulin an endogenous cardioprotector? Presented without comment, except to say that hyperinsulinemia is not the problem, it's what causes the hyperinsulinemia.  That being insulin resistance!

Having been introduced to "the English guy" aka Keith Frayn, I've discovered a rather extensive, as well as diverse, body of work by this researcher.   I'm sure to be sharing more in the coming weeks.   Visceral fat and insulin resistance – causative or correlative?   (link is to full-text PDF) The association between abdominal fat accumulation and risk of chronic diseases, including type II diabetes and coronary heart disease, has long been recognized. Insulin resistance may be a key factor in this link. Many studies have pointed to an association between insulin resistance and intra-abdominal fat accumulation (visceral obesity). However there is no clear proof of a causal link between visceral fat accumulation and insulin resistance. In assessing the probability of a causal link, it is useful to consider potential mechanisms. One such potential causal link is the release of non-esterified fatty acids from visceral fat into the portal ...

Mostly a bookmarking post, but I found this interesting Substituting dietary saturated fat with polyunsaturated fat changes abdominal fat distribution and improves insulin sensitivity For some reason I can't C&P the abstract. They analyzed the results of 5 weeks on diets rich in sat fat vs. PUFA (described as spreads and oils, presumably high in omega 6 and probably some transfats :( ) on T2's, obese and non-obese subjects.  The study size was small, but I think most readers will be as surprised as I was by the results. All of the PUFA groups had less subcutaneous belly fat at the end of the 5 weeks. This was statistically significant in the non-diabetics, both obese and non-obese.  Visceral fat either decreased or stayed the same. This was statistically significant for the diabetics, but not the non-diabetics.   The PUFA group seemed to eat less, but total body weight didn't change.  Not sure what that's about.  Could be underreporting or a slower m...

Effects of Omega-3 Fatty Acids on Lipids Glycemic Control in Type II Diabetes and the Metabolic Syndrome and on Inflammatory Bowel Disease, Rheumatoid Arthritis, Renal Disease, Systemic Lupus Erythematosus, and Osteoporosis           Summary This is a summary of all the research this group could find about O3's.  Just putting this here to bookmark and FYI.

James Kreiger just posted his final chapter in his series on insulin.  If you don't want to read the entire series, I highly recommend reading this last installment that summarizes all points. Insulin, An Undeserved Bad Reputation: The Finale

WOW, just realized how long this is!  Sorry!! OK folks.  I've waited a couple of days here to see if I would get another email from GT before posting an update on our exchange.  No further emails, so here's the scoop dear readers. In response to some of my recent posts, GT initiated an email exchange with me.  I don't really participate in private email exchanges over science stuff unless there's an understanding that I can share what is discussed.  Why?  Because anything of some utility to me, would be of no utility to others if I can't share it.  Then I'm left in the precarious situation of deciding what content/info I may wish to share on my blog.    It's highly wasteful of my time to respond separately in private and public venues, so I would rather use my time more wisely. At the end of his initial email, GT stated that I could share the email so long as I did so in full.  I took this to mean that GT was interested in "open sha...

Glyceroneogenesis Is the Dominant Pathway for Triglyceride Glycerol Synthesis in Vivo in the Rat* OK ... yes, this is a rat study, but the body of work by Hanson's group has demonstrated that the results obtained for the rat correlate well with human metabolism.  These studies utilized radiolabeling "tracer" methods to track the substrate source for G3P.  Three dietary groups were compared: 1.  Controls - regular chow fed (removed 7am study morning) 2.  48 hour fasted (food removed 48 hrs prior) 3.  Lipogenic (high sucrose) diet (5 day sucrose water in addition to regular chow and glucose infusion during testing to "maintain the lipogenic state"). The abstract is long so I'll let y'all readers just read it at the source if you like.  I'll focus this post on excerpts from the discussion of the results. Plasma:   The plasma concentration of triglyceride were not different in the three groups ( Table 1 ). The fraction of plasma triglyceride glycero...

I just got around to reading Matt Stone's excellent Befriending Insulin  post.   I highly recommend it to all my readers.  I have a few factual issues with it (have been trying to comment there but will email Matt shortly), but on the whole it is solid.  FWIW, I'm not so sure I could embrace Matt's methods of "undoing" VLC (I'm not into gaining ANY weight), but that's irrelevant, IMO, to the discussion. I came late to the online LC party, relying mostly on my memory of Atkins Induction to fashion my plan beginning sometime summer 2007.  I remember when I first started reading on the web something just didn't ring true to me about insulin and the way it was being demonized.  Where did this come from, I wondered.  Insulin deficiency is a bad thing.  It leads to elevated NEFA as well as hyperglycemia.   I've blogged on the vascular actions of insulin that are positive in nature.  So why would our goal be to achieve this state?   As M...

Relationship between Adipocyte Size and Adipokine Expression and Secretion Context : Adipocytes are known to release a variety of factors   that may contribute to the proinflammatory state characteristic   for obesity. This secretory function is considered to provide the basis for obesity-related complications such as type 2 diabetes   and atherosclerosis. Objective : To get a better insight into possible underlying   mechanisms, we investigated the effect of adipocyte size on   adipokine production and secretion. Design, Patients, and Main Outcome Measures : Protein secretion   and mRNA expression in cultured adipocytes separated according   to cell size from 30 individuals undergoing elective plastic   surgery were investigated. Results : The mean adipocyte volume of the four fractions ranged   from 205 ± 146 to 1.077 ± 471 pl. There were strong linear correlations for the secretion of adipokines over time.   Secr...

Here's one paper by Hall and Chow, or the duo my readers might recognize as those young biophysicists.  This link is to the free full text. The Dynamics of Human Body Weight Change Abstract:   An imbalance between energy intake and energy expenditure will lead to a change in body weight (mass) and body composition (fat and lean masses). A quantitative understanding of the processes involved, which currently remains lacking, will be useful in determining the etiology and treatment of obesity and other conditions resulting from prolonged energy imbalance. Here, we show that a mathematical model of the macronutrient flux balances can capture the long-term dynamics of human weight change; all previous models are special cases of this model. We show that the generic dynamic behavior of body composition for a clamped diet can be divided into two classes. In the first class, the body composition and mass are determined uniquely. In the second class, th...

I've received a few behind the scenes comments regarding my use and choice of pseudonym and the names of my blogs.    More specifically, some have expressed that my use of the word "sane" is somehow insulting to low carbers because it implies that more restrictive LC WOE's are somehow insane.  Well, that is not my intent, although I do see a faction in the LC community exhibiting the same sort of zealotry as the LF community did/does.   I had originally intended to do just one blog before separating it into science and personal.  The Sane-Asylum is (obviously) a play on words on insane asylums.  Asylum is refuge or a safe place.  I consider myself to be in such a place as regards my relationship with and attitude towards carbohydrates.  While it may seem like I post a lot of "anti-LC" stuff here, that is not really my intent.  I'm looking for the best way forward, no matter where that leads.  I do, however, hope to foster an environmen...

I was recently invited by Jimmy Moore to appear on his podcast in response to some of my recent posts on Gary Taubes' most recent lecture and his interview with Jimmy.  This elicited the following email to me from Gary Taubes.  (Aside:  My email is open to anyone who wishes to use it through my profile here).  At his request, I have included it in its entirety here along with my responses.  Taubes' words are in default font, my responses are in green italics. ************************************************ Hi Carb Sane,    I hope you don't mind me taking the liberty of e-mailing you. Jimmy Moore told me that you might be going on his show,  which prompted me to try to read a few of your latest blog entries. Occasionally, friends have suggested I read and respond to your critiques (attacks?) , but whenever I try I find them tough going. Your descriptions of what I wrote or said or argued never quite seem to mesh with what I actually wrote or s...