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AMP-Activated Protein Kinase, AMPK
"AMP-activated protein kinase (AMPK) was first discovered as an activity that inhibited preparations of acetyl-CoA carboxylase (ACC) and 3-hydroxy-3-methylglutaryl-CoA reductase (HMG-CoA reductase, HMGR) and was induced by AMP. AMPK induces a cascade of events within cells in response to the ever changing energy charge of the cell. The role of AMPK in regulating cellular energy charge places this enzyme at a central control point in maintaining energy homeostasis. More recent evidence has shown that AMPK activity can also be regulated by physiological stimuli, independent of the energy charge of the cell, including hormones and nutrients.
Once activated, AMPK-mediated phosphorylation events switch cells from active ATP consumption (e.g. fatty acid and cholesterol biosynthesis) to active ATP production (e.g. fatty acid and glucose oxidation). These events are rapidly initiated and are referred to as short-term regulatory processes. The activation of AMPK also exerts long-term effects at the level of both gene expression and protein synthesis. Other important activities attributable to AMPK are regulation of insulin synthesis and secretion in pancreatic islet β-cells and modulation of hypothalamic functions involved in the regulation of satiety. How these latter two functions impact obesity and diabetes will be discussed below. "
AMP-activated protein kinase - Wikipedia, the free encyclopedia
"5' AMP-activated protein kinase or AMPK or 5' adenosine monophosphate-activated protein kinase is an enzyme that plays a role in cellular energy homeostasis. It consists of three proteins (subunits) that together make a functional enzyme, conserved from yeast to humans. It is expressed in a number of tissues, including the liver, brain, and skeletal muscle. The net effect of AMPK activation is stimulation of hepatic fatty acid oxidation and ketogenesis, inhibition of cholesterol synthesis, lipogenesis, and triglyceride synthesis, inhibition of adipocyte lipolysis and lipogenesis, stimulation of skeletal muscle fatty acid oxidation and muscle glucose uptake, and modulation of insulin secretion by pancreatic beta-cells.[1]
It should not be confused with cyclic AMP-activated protein kinase (protein kinase A), which, although being of similar nature, may have opposite effects.[2]"
GNC - HealthNotes
"Healthnotes offers comprehensive, science-based health and lifestyle information. Written with you in mind, Healthnotes answers the most commonly asked questions with credible, easy-to-understand information. Healthnotes' content is edited by physicians who review over 550 scientific and medical journals to keep content current, factual, and balanced. Articles include footnotes tied to over 14,000 references. "
The hypoglycemic effect of fat and protein is not attenuated by insulin resistance -- Lan-Pidhainy and Wolever 91 (1): 98 -- American Journal of Clinical Nutrition
The hypoglycemic effect of fat and protein is not attenuated by insulin resistance.
Lan-Pidhainy X, Wolever TM.
Am J Clin Nutr. 2009 Nov 18. [Epub ahead of print]
PMID: 19923374
doi:10.3945/ajcn.2009.28125
Conclusions: The hypoglycemic effect of fat and protein was not blunted by insulin resistance. Protein increased insulin but had no effect on C-peptide or the insulin secretion rate, which suggests decreased hepatic insulin extraction or increased C-peptide clearance.
Defensin - Wikipedia, the free encyclopedia
"Defensins are small cysteine-rich cationic proteins found in both vertebrates and invertebrates. They are active against bacteria, fungi and many enveloped and nonenveloped viruses. They consist of 18-45 amino acids including six (in vertebrates) to 8 conserved cysteine residues. Cells of the immune system contain these peptides to assist in killing phagocytized bacteria, for example in neutrophil granulocytes and almost all epithelial cells. Most defensins function by binding to microbial cell membrane, and once embedded, forming pore-like membrane defects that allow efflux of essential ions and nutrients
Coconut kernel protein modifies the effect of coconut oil on serum lipids. - Plant Foods Hum Nutr. 1999 - SpringerLink - Journal Article
Coconut kernel protein modifies the effect of coconut oil on serum lipids.
Padmakumaran Nair KG, Rajamohan T, Kurup PA.
Plant Foods Hum Nutr. 1999;53(2):133-44.
PMID: 10472790
DOI: 10.1023/A:1008078103299
Feeding coconut kernel along with coconut oil in human volunteers has been found to reduce serum total and LDL cholesterol when compared to feeding coconut oil alone. This effect of the kernel was also observed in rats. Since many plant proteins have been reported to exert a cholesterol lowering effect, a study was carried out on the effect of isolated kernel protein in rats. Feeding kernel protein resulted in lower levels of cholesterol, phospholipids and triglycerides in the serum and most tissues when compared to casein fed animals. Rats fed kernel protein had (1) increased hepatic degradation of cholesterol to bile acids, (2) increased hepatic cholesterol biosynthesis, and (3) decreased esterification of free cholesterol. In the intestine, however, cholesterogenesis was decreased. The kernel protein also caused decreased lipogenesis in the liver and intestine. This beneficial effect of the kernel protein is attributed to its very low lysine/arginine ratio 2.13% lysine and 24.5% arginine....
Effect of soy protein varying in isoflavone content on serum lipids in healthy young men -- McVeigh et al. 83 (2): 244 -- American Journal of Clinical Nutrition
Effect of soy protein varying in isoflavone content on serum lipids in healthy young men.
McVeigh BL, Dillingham BL, Lampe JW, Duncan AM.
Am J Clin Nutr. 2006 Feb;83(2):244-51.
PMID: 16469981
Conclusion: Soy protein, regardless of isoflavone content, modulates serum lipid ratios in a direction beneficial for cardiovascular disease risk in healthy young men.
Therapeutic applications of whey protein - 136.pdf (application/pdf Object)
Marshall K.
Therapeutic applications of whey protein.
Altern Med Rev. 2004 Jun;9(2):136-56. Review.
PMID: 15253675
Klotho (biology) - Wikipedia, the free encyclopedia
"The Klotho gene codes for a transmembrane protein that, in addition to other effects, provides some control over the sensitivity of the organism to insulin and appears to be involved in aging. Its discovery was documented in 1997 by Kuro-o et al.[1] The name of the gene comes from Klotho or Clotho, one of the Moirae, or Fates, in Greek mythology.
The Klotho protein is a novel β-glucuronidase (EC number 3.2.1.21) capable of hydrolyzing steroid β-glucuronides. Genetic variants in KLOTHO have been associated with human aging,[2] and Klotho protein has been shown to be a circulating factor detectable in serum that declines with age.[3]
Klotho-deficient mice manifest a syndrome resembling accelerated human aging"
FAQ - Australian Homo Optimus Society Homepage - cybernaut.com.au
No one can dispute that mother's milk is the ideal nutrition, as far as the biochemical composition is concerned. It contains 3 to 11 grams of fat per 1 gram of protein (0.4% unsaturated fat). The conclusion is obvious - if Nature included such a minute quantity of that constituent in such a wonderful food, then we should respect it. Meanwhile, people are being persuaded that plant-derived fats containing polyunsaturated fatty acids which do not exist in mother's milk, are healthy. Nothing is more misleading.
The best are the fats which contain the highest percentage of energy contributing constituents, or in other words, such in which COOH group is attached to the longest fatty acid chain. Short fatty acid chains contain around 30-40% of energy-contributing constituents, the longest ones over 90%.
Long-chain fatty acids fully saturated with hydrogen, yields approx. 10 cal/g when metabolised, the same as petrol. Fat's value as a "fuel" for our body increases with the increase in the amount of hydrogen per gram of carbon in its molecule, with the increase in the energy-contributing constituents.
Chemically, the best are long-chain fully saturated fatty acids, that is to say, solid fats of animal origin. Only fats with the length of the chain above 10 carbon atoms are suitable to be utilised by our cells and tissues without conversion. These fats are directed straight to the blood stream via the lymphatic system, and they do not have to be converted and made suitable by the liver, as is the case with inferior fats (with shorter chains), or all other constituents of consumed and digested foods
Australian Homo Optimus Society Homepage - www.cybernaut.com.au
"Dr Jan Kwasniewski
This Website is dedicated to Dr Jan Kwasniewski who has spent his lifetime developing and using the Optimal Diet bringing health and happiness to many people.
Dr Jan Kwasniewski still lives in Poland, he has refused to commercialise his development and is not a very rich person. He does not sell any supplements. Compared with the standards enjoyed by Western medicos he lives a very ordinary, modest life."
Homo Diet Healthy Way of Eating, by Dr. Jan Kwasniewski - homodiet.netfirms.com
Welcome to the English language website for the "Optimal Diet" movement. The Optimal Diet is a dietary model of human nutrition devised and implemented by Dr. Jan Kwasniewski. The Optimal Diet is a movement, which originated in recent years in Poland, and has rapidly spread to a number of countries worldwide, is to improve the well-being, health and biological value of people as individuals, and to correct nutritional mistakes of human kind as a whole, through promotion and implementation of the "optimal" model of human nutrition.
Optimal Diet is based on the delivery of the most important nutritional elements, e.g., the most valuable proteins and fats, whilst leaving the body in charge of the distribution of these elements to the most critical areas.
The ideal proportion between the main food components of protein, fat and carbohydrates should be in the range of :
m m m m 1 : 2.5 - 3.5 : 0.5
In order to work out the correct daily food intake using this proportion, one has to know how many grams of protein needs to be ingested in a day to satisfy body's requirements.
Ketogenic diets and physical performance - Nutrition & Metabolism | Full text
Ketogenic diets and physical performance.
Phinney SD.
Nutr Metab (Lond). 2004 Aug 17;1(1):2.
PMID: 15507148
doi:10.1186/1743-7075-1-2
Impaired physical performance is a common but not obligate result of a low carbohydrate diet. Lessons from traditional Inuit culture indicate that time for adaptation, optimized sodium and potassium nutriture, and constraint of protein to 15–25 % of daily energy expenditure allow unimpaired endurance performance despite nutritional ketosis.
Both observational and prospectively designed studies support the conclusion that submaximal endurance performance can be sustained despite the virtual exclusion of carbohydrate from the human diet. Clearly this result does not automatically follow the casual implementation of dietary carbohydrate restriction, however, as careful attention to time for keto-adaptation, mineral nutriture, and constraint of the daily protein dose is required. Contradictory results in the scientific literature can be explained by the lack of attention to these lessons learned (and for the most part now forgotten) by the cultures that traditionally lived by hunting. Therapeutic use of ketogenic diets should not require constraint of most forms of physical labor or recreational activity, with the one caveat that anaerobic (ie, weight lifting or sprint) performance is limited by the low muscle glycogen levels induced by a ketogenic diet, and this would strongly discourage its use under most conditions of competitive athletics.
Calbindin - Wikipedia, the free encyclopedia
"Calbindin describes calcium binding proteins first described as the vitamin D-dependent calcium binding proteins in intestine and kidney."
Vitamin D-dependent calcium-binding protein - Wikipedia, the free encyclopedia
"Vitamin D-dependent calcium binding proteins were discovered in the cytosolic fractions of chicken intestine, and later in mammalian intestine and kidney, by workers including Robert Wasserman of Cornell University.
They bound calcium in the micromolar range and were greatly reduced in vitamin D-deficient animals. Expression could be induced by treating these animals with vitamin D metabolites such as calcitriol.
They were found to exist in two distant sizes with a molecular weight of approximately 9 kDa and 28 kDa. They were renamed calbindin; calbindin-D9k is found in mammalian intestine and calbindin-D28k in avain intestine and in kidney."
Egg yolk proteins suppress azoxymethane-induced aberrant crypt foci formation and cell proliferation in the colon of rats
Egg yolk proteins suppress azoxymethane-induced aberrant crypt foci formation and cell proliferation in the colon of rats.
Ishikawa S, Asano T, Takenoshita S, Nozawa Y, Arihara K, Itoh M.
Nutr Res. 2009 Jan;29(1):64-9.
PMID: 19185779
These results indicate that dietary egg yolk proteins have a preventive effect on AOM-induced large bowel carcinogenesis in rats; it exerts this effect by altering cell proliferation through SCFA production. This study suggests that the consumption of egg yolk proteins might be protective against colon carcinogenesis.
Dietary Cod Protein Reduces Plasma C-Reactive Protein in Insulin-Resistant Men and Women -- Ouellet et al. 138 (12): 2386 -- Journal of Nutrition
Dietary cod protein reduces plasma C-reactive protein in insulin-resistant men and women.
Ouellet V, Weisnagel SJ, Marois J, Bergeron J, Julien P, Gougeon R, Tchernof A, Holub BJ, Jacques H.
J Nutr. 2008 Dec;138(12):2386-91.
PMID: 19022962
Therefore, these results show that CP can lower hsCRP, a marker of inflammation associated with insulin resistance and type 2 diabetes.
Dietary Cod Protein Improves Insulin Sensitivity in Insulin-Resistant Men and Women - Diabetes Care
Dietary cod protein improves insulin sensitivity in insulin-resistant men and women: a randomized controlled trial.
Ouellet V, Marois J, Weisnagel SJ, Jacques H.
Diabetes Care. 2007 Nov;30(11):2816-21. Epub 2007 Aug 6.
PMID: 17682120
CONCLUSIONS - Dietary cod protein improves insulin sensitivity in insulin-resistant individuals and thus could contribute to prevention of type 2 diabetes by reducing the metabolic complications related to insulin resistance.
Prevention of skeletal muscle insulin resistance by dietary cod protein in high fat-fed rats -- Lavigne et al. 281 (1): E62 -- AJP - Endocrinology and Metabolism
Prevention of skeletal muscle insulin resistance by dietary cod protein in high fat-fed rats.
Lavigne C, Tremblay F, Asselin G, Jacques H, Marette A.
Am J Physiol Endocrinol Metab. 2001 Jul;281(1):E62-71.
PMID: 11404223
These data demonstrate that feeding cod protein prevents obesity-induced muscle insulin resistance in high fat-fed obese rats at least in part through a direct action of amino acids on insulin-stimulated glucose uptake in skeletal muscle cells.
Diet, evolution and aging--the pathophysiologic effects of the post-agricultural inversion of the potassium-to-sodium and base-to-chloride ratios in the human diet - Eur J Nutr. 2001 Oct;40(5):200-13 - SpringerLink - Journal Article
Diet, evolution and aging--the pathophysiologic effects of the post-agricultural inversion of the potassium-to-sodium and base-to-chloride ratios in the human diet.
Frassetto L, Morris RC Jr, Sellmeyer DE, Todd K, Sebastian A.
Eur J Nutr. 2001 Oct;40(5):200-13. Review.
PMID: 11842945
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