Showing posts from April, 2010

Insulin Response of Long Term Type 2 Diabetics Improved with Amino Acids

Amino Acid Ingestion Strongly Enhances Insulin Secretion in Patients With Long-Term Type 2 Diabetes ABSTRACT: OBJECTIVE—Insulin secretion in response to carbohydrate intake is blunted in type 2 diabetic patients. However, it is not clear whether the insulin response to other stimuli, such as amino acids, is also diminished. Recently, we defined an optimal insulinoptropic mixture containing free leucine, phenylalanine, and a protein hydrolysate that substantially enhances the insulin response in healthy young subjects when coingested with carbohydrate. In this study, we aimed to investigate the insulinotropic capacity of this mixture in long-term type 2 diabetic patients. RESEARCH DESIGN AND METHODS—Ten type 2 diabetic patients (aged 59.1 ± 2.0 years, BMI 26.5 ± 0.7 kg/m 2 ) and 10 healthy control subjects (58.8 ± 2.1 years, 26.5 ± 0.7 kg/m 2 ) visited our lab twice, during which insulin responses were determined following ingestion of carbohydrate only (CHO) or carbohydr

More Biochemistry Animations

Boyer - Interactive Biochemistry A screen shot of the Menu:

A Neat Gluconeogenesis Tutorial

Interactive Gluconeogenesis Tutorial

Effects of aerobic exercise and dietary carbohydrate on energy expenditure and body composition during weight reduction in obese women

Effects of aerobic exercise and dietary carbohydrate on energy expenditure and body composition during weight reduction in obese women My Summary: Subjects:  23 Obese (44 +/- 4% BF), Healthy, Premenopausal Women (Range 21-47, late 30's on average)  Compared:  Two diets -- one low fat LF , one low carb LC,  and Two exercise states -- one aerobic EX, one no exercise  NX -- Four groups were compared LF/NX, LF/EX, LC/NX, LC/EX. Study Length:  12 Weeks of weight loss, preceded by 5 weeks maintenance (MI), and followed by 6 weeks maintenance (MII). Diets - Carb/Protein/Fat:  Maintenance - 45/20/35 ; LC - 25/25/50 ; LF - 60/25/15  It is worth noting that the LC vs. LF comparison kept protein constant.  The caloric content of the reducing diets was individualized to each participant to be ~75% of measured RMR. Exercise:   3X/week, 45 minutes = 15 min on each of three different cardio machines, 60-65% VO2max Measured:  Changes in body composition, Resting Metabolic Rate (RMR), the


Glyceroneogenesis and the Source of Glycerol for Hepatic Triacylglycerol Synthesis in Humans Glyceroneogenesis, i.e . the synthesis of the glycerol moiety of triacylglycerol from pyruvate, has been suggested to be quantitatively important in both the liver and adipose tissue during fasting. However, the actual contribution of glyceroneogenesis to triacylglycerol synthesis has not been quantified in vivo in human studies. In the present study we have measured the contribution of glycerol and pyruvate to in vivo synthesis of hepatic triacylglycerol in nonpregnant and pregnant women after an overnight fast.  After a 16-h fast, ∼6.1% of the plasma triacylglycerol pool was derived from plasma glycerol, whereas 10 to 60% was derived from pyruvate in nonpregnant women and pregnant women early in gestation. Our data suggest that glyceroneogenesis from pyruvate is quantitatively a major contributor to plasma triacylglycerol synthesis and may be important for the regulation o

PEPCK Website There's some interesting information on this -- apparently -- "amateur" website.  PEPCK is an important enzyme regulating blood glucose and free fatty acid levels.  It is involved in gluconeogenesis and glyceroneogenesis.

Ketones, Anaplerosis & Insulin

Acetoacetate and β-hydroxybutyrate in combination with other metabolites release insulin from INS-1 cells and provide clues about pathways in insulin secretion Putting this here for my own orgnization Conclusions: The synergistic insulin release by compounds that can be metabolized to mitochondrial acetyl-CoA, such as KIC, β-hydroxybutyra te, or acetoacetate, in combination with methyl succinate that can be metabolized to mitochondrial oxaloacetate, suggests that acetyl-CoA and oxaloacetate condense in the citrate synthase reaction to form citrate. Numerous compounds can be formed from citrate, and citrate can carry acetyl-CoA and oxaloacetate out of the mitochondria to the cytosol. Many compounds, including most short-chain acyl-CoAs, can be formed from acetyl-CoA in the cytosol. KIC and β-hydroxybutyra te can also be directly converted to acetoacetate and acetyl-CoA in the mitochondria. Acetoacetate can be exported to the cytosol and converted to acetoacetyl-CoA to

Protein in optimal health: heart disease and type 2 diabetes

Protein in optimal health: heart disease and type 2 diabetes Aside:  The lead author (I believe), is affiliated with the Australian CSIRO research group that is well regarded in the LC community -- except when, in the end, CSIRO's highly successful weight loss plan does not advocate for high fat  VLC after all.  I would also point out that the authors and the summit from which this article originated were highly subsidized by "Big Egg", "Big Dairy", "Big Beef" and "Big Pork".  I point this out not because I question the findings that seem pretty sound, but to point out that discounting research based on the sponsor just because one doesn't like the outcome is common practice amongst "debunkers". So, that said, on to this article.  I won't repeat the whole thing.  It is a review, and although requires slow reading to digest, it's not overly clouded with technical lingo.  Some highlights of interest in no particular ord

Soluble Fiber and Net Carbs

I believe that, like sugar alcohols, soluble dietary fiber should be counted on a 0.5g carb/gram fiber basis.  However since most dietary fiber is not listed as to whether it is soluble or insoluble, this can be difficult to do.  Erring on the side of caution, a 1g for every 3g total dietary fiber would be a good compromise.  But many of the LC "fibers" such as polydextrose, inulin and glucomannan (shiritaki noodles) are essentially all soluble so 1g counted for 2g is a better count. In soluble dietary fiber, IDF, passes through the human digestive system unchanged so it is non-nutritive in all aspects. Further, since it adds bulk to food and assists in stool formation and "moving things along" IDF can reduce the nutrient absorbtion from the food we do eat.  This is essentially the rap of the "fiber is overrated" contingent. SDF may not be metabolized by the body, but it is fermented by intestinal bacteria to short chain fatty acids (SCFA

Fatty Acid Contents of Foods: Beef Fat vs. Seal Oil

Another random listing from fatty acid compositions at This post was precipitated by the oft cited Inuit as an example of the benefit of an almost all "meat", very high fat diet.  I've noticed that many of those practicing this version of a "Paleolithic" diet, tend to consume a lot of beef and rarely eat even the fish which are another staple of the Inuit diet.  So I decided to compare beef fat to that in seal oil.  The contrasts are quite stark!!

Fatty Acid Contents of Foods: Butter & Coconut Oil

On occasion I look up this type of info on -- it comes from the pull-down analysis of the fats.  This is for one ounce (28g) of butter.  (NOTE:  I suspect there is an error here on the serving size vs. fat content.  Normally 1T butter has ~11g total fat) Of note, a little more than 3% (~1/2 g) of the total fat is butyric acid, the short chain fatty acid product that is the byproduct of some soluble fiber metabolism.  Butter also contains 3.6% of capric and caprylic acids combined -- these are the 8 & 10 carbon medium chain triglycerides in "MCT oil".  Lauric acid (12C)  is 2.7% (this is the longest chain length characterized as medium chain, that is almost 50% of the fatty acid content of coconut oil).  All in all, the short and medium chain triglyceride content of butter is 11.6%, of which ~8.4% are classified as MCT's.  By contrast, coconut oil (source: wikipedia) is a little more than 60% MCT's. The PUFA's are all Omega 6

Apoptosis - Programmed Cell Death

Here is a link to a website dedicated to Apoptosis/PCD:   Apoptosis Apoptosis is the term given when programmed cell death (PCD) occurs in multicellular organisms. Apoptosis is one of the main types of programmed cell death which involves a series of biochemical events leading to specific cell morphology characteristics and ultimately death of cells. Characteristic cell morphology of cells undergoing apoptosis include blebbing, changes to the cell membrane such as loss of membrane asymmetry and attachment, cell shrinkage, nuclear fragmentation, chromatin condensation, and chromosomal DNA fragmentation. Apoptosis differentiates from necrosis as the processes associated with apoptosis in disposal of cellular debris do not damage the organism in apoptosis. Necrosis is a form of traumatic cell death that results from acute cellular injury. Apoptosis in contrast to necrosis, confers advantages during an organism's life cycle. For instance during the development of t

Long term exposure to fatty acids and ketones inhibits B-cell functions in human pancreatic islets of Langerhans

Long term exposure to fatty acids and ketones inhibits B-cell functions in human pancreatic islets of Langerhans We previously demonstrated in the rat that long term exposure to fatty acids inhibits B-cell function in vivo and in vitro. To further assess the clinical significance of these findings, we tested in human islets the effects of fatty acids on glucose-induced insulin release and biosynthesis and on pyruvate dehydrogenase (PDH) activity. PDH is the enzyme thought to control the entry of acetyl CoA from glycolysis into the Kreb's / TCA /Citric Acid Cycle. These authors did an in vitro  study with human cells to see if the results compared with those seen both in vitro and in vivo  in rats.  While in vitro  observations don't always correlate with what we see in whole organisms, this did correlate for the rat.  Therefore it is reasonable to believe that the results of this experiment are applicable to human metabolism. Human islets were obtained from the β-Cell

Glyceroneogenesis and the Triglyceride/Fatty Acid Cycle

Everyone who believes Taubes' theories about Glycerol-3-P and not being able to store fat if you don't ingest dietary carbs should read this article. Glyceroneogenesis and the Triglyceride/Fatty Acid Cycle We make glucose via gluconeogenesis.  So, too, we make glycerol via glyceroneogenesis.  And we recycle ~50-65% of the FA's released via lipolysis back to trigs. One interesting thing is the behavior of brown adipose tissue.  The enzyme responsible for re-esterification, PEPCK-C is high in BAT.  But interestingly enough insulin INHIBITS this enzyme while a high protein zero carb diet stimulates it.   There's lots more  here to digest.  I'll revisit this post and update.

Glycogen storage capacity and de novo lipogenesis during massive carbohydrate overfeeding in man

Glycogen storage capacity and de novo lipogenesis during massive carbohydrate overfeed ing in man. ABSTRACT:   The metabolic balance method was performed on three men to investigate the fate of large excesses of carbohydrate. Glycogen stores, which were first depleted by diet (3 d, 8.35 ± 0.27 MJ [1994 ± 65 kcal] decreasing to 5.70 ± 1.03 MJ [1361 ± 247 kcal], 15% protein, 75% fat, 10% carbohydrate) and exercise, were repleted during 7 d carbohydrate overfeeding (11% protein, 3% fat, and 86% carbohydrate) providing 15.25 1. 10 MJ (3642 ± 263 kcal) on the first day, increasing progressively to 20.64 ± 1 .30 MJ (4930 ± 3 1 1 kcal) on the last day of overfeeding. Glycogen depletion was again accomplished with 2 d of carbohydrate restriction (2.52 MJ/d [602 kcal/d], 85% protein, and 15% fat). Glycogen storage capacity in man is ~15 g/kg body weight and can accommodate a gain of ~500 g before net lipid synthesis contributes to increasing body fat mass. When the glycogen stores are saturate