Altri attivatori dell'AMPK:
- la contrazione muscolare attiva l'AMPK http://www.ncbi.nlm.nih.gov/pubmed/17997341
- adiponectina http://www.ncbi.nlm.nih.gov/pubmed/20667975
- inibizione del sistema nervoso simpatico http://www.ncbi.nlm.nih.gov/pubmed/18269175
Il primo punto si commenta da solo, per gli ultimi due la taurina è il candidato ideale.
http://www.ncbi.nlm.nih.gov/pubmed/8915402
http://www.ncbi.nlm.nih.gov/pubmed/17080243
Aggiungo il fondamentale studio del gruppo di Yukio Yamori sul rapporto tra alimentazione (taurina e magnesio in particolare) e malattie cardiovascolari. Non perdevetelo!
http://www.jbiomedsci.com/content/17/S1/S6
We are still continuing our CARDIAC health examination since we started the world wide study in 1985 in coordination with WHO. Our recent study on Australian Aboriginal people for over past 7 years demonstrated that they are presently suffering most severely from lifestyle-related diseases in comparison with the other CARDIAC populations [38,45]. Obesity, hypertension and diabetes in Aboriginals start 20 to 30 years younger than other Australian and Japanese people (Figure 10) [45]. When they lost bush food, their M intake was greatly decreased because bush food consisting of nuts, seeds, grains, beans, fruits and seaweeds contains much M (Figure 11). Aboriginals living near the coast of the state of Victoria used to utilize various foods from the sea and fresh water. Aboriginals living in Framlingham, Victoria were known to start the culture of eels 8,000 years ago and there were several large shell mounds, the piling up of various shells like mountains at the sea side not far from Melbourne, indicating that Aboriginals’ life had been highly dependent on their bush food as well as on the seafood, both the richest sources of T and M. Before the colonials were established, their daily foods were clams, various shells and fish containing a large amount of T (Figure 12), and also their traditional smoked eels, which were a rich source of T and DHA and eaten as their common preserved food. As hunters and food gatherers, Aboriginals, according to the 2-week food intake analysis report, were supposed to live by taking their energy, for example, 34% from complex carbohydrates, 13% from fat and 53% from protein [46]. Although we do not know exactly what they ate, we tentatively suppose, for example, they ate 400 g of yam, 300 g of frogs, 5 g of almonds, 140 g of bream, 200 g of clams, 300 g of snails. These foods contain about 100 g of carbohydrates, 15 g of fat and 170 g of protein and correspond roughly to 1300 kcal/day. The daily intake of T and M from these foods is about 3200 mg and 640 mg, respectively, both being far higher than the average of CARDIAC populations in the world.
3 grammi di taurina e 600 mg di magnesio al giorno! Alla faccia dei disclaimer sui barattoli di taurina. [
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Both T and M are basically important for the maintenance of life. T is involved in cellular physiology by its effect on osmoregulation, anti-oxidant, membrane stabilization and calcium regulation [47-49], and also on lipid metabolism related to dyslipidemia and atherosclerosis through its role in bile acid conjugation [47,48]. Recently, T-conjugated endogenous bile acid derivative, ursodeoxycholic acid was focused on as a chemical chaperone which was proven to reduce endoplasmic reticulum (ER) stress and restore glucose homeostasis in a mouse model of type 2 diabetes [50]. The alleviation of ER-stress may restore insulin sensitivity in the liver, muscle and adipose tissue, thus contributing to the resolution of fatty liver diseases, diabetes and obesity. High dietary T administration was proven to reduce apoptosis and atherosclerosis possibly via normalization of ER stress [51].
Moreover, in relation to the ageing of vascular tissue and the accelerated senescence of endothelial progenitor cell (EPC) noted in SHRSP [52], T was reported to attenuate EPC senescence in SHRSP and to modulate clinically the deterioration of endothelial function in smokers [53-55]. These classical and new concepts of the pathophysiological roles of T suggest that a high T intake may contribute to longevity through CVD health and lifestyle-related diseases.
On the other hand, M is the 8th abundant element in the weight, the number of atoms and the volume percentage of all atoms on the earth. It is also the most abundant intracellular divalent cation and is involved in the various biological functions of about 300 enzymes as their coenzyme. They include all enzymatic reactions requiring ATP, such as Na-K ATPase, important for intracellular ionic balance. Therefore, M is supposed to be causatively and clinically related to cardiovascular health, hypertension and diabetes [56-58]. Lowering of intracellular free M was observed in SHRSP in the process of aging and development of hypertension [59]. Dietary M supplementation increased intralymphocytic free M and attenuated the grade of hypertension [60]. These experimental findings were recently confirmed clinically in patients with mild hypertension whose ambulatory BP was significantly decreased concomitantly with the increased intracellular free M and K, and decreased intracellular free Ca and Na, by the dietary supplementation of 600 mg of pidolate M [61]. In this clinical experiment, M supplementation increased serum M and 24U excretion of M. Therefore, the aforementioned epidemiologically observed 24U-M excretion was regarded to correspond to dietary M intake. M was also reported to decrease BP by inhibiting sympathetic nerve by blocking N-type Ca channels [62].
Since the evolutional origin of life of human beings was inside the sea containing abundant M and food gatherers lived on seafood rich in T, both M and T are assumed to be essential for the homeostasis maintaining cardiovascular health.
