massamagra/colesterolo-hdl-ldl-trigliceridi.htm

1. http://www.massamagra.com/colesterolo-hdl-ldl-trigliceridi.htmhttp://www.massamagra.com/colesterolo-hdl-ldl-trigliceridi.htm IL COLESTEROLOIl colesterolo è una molecola rigida con molte importanti funzioni. Serve tra l’altro a conferire rigidità alle membrane cellulari di tutto il regno animale. Le membrane sono costituite da un doppio strato di molecole chiamate “fosfolipidi”, cioè grassi (insolubili) legati ad un gruppo fosforico (solubile), che si dispongono a palizzata per formare la membrana. Questo doppio strato è estremamente fluido, ed il colesterolo serve a conferire rigidità e a permettere la formazione di strutture più resistenti. Senza colesterolo non esisteremmo. Il corpo non potrebbe, per esempio, replicare le cellule perché non avrebbe la sostanza base. Senza abbastanza colesterolo il nostro organismo non potrebbe rimpiazzare le cellule morte della pelle, non sarebbe in grado di rinnovare i tessuti, le unghie, i capelli, non sarebbe in grado di riparare i muscoli e non potrebbe rinnovare l’intera superficie intestinale ogni 4 giorni, per esempio.

2. Il Colesterolo presente nel sangue è prodotto per l’80% dal fegato, mentre il restante 20% lo si ricava dagli alimenti. Il Colesterolo (che non è un grasso ma un alcole, come la cera) non è solubile, ed ha quindi bisogno di speciali proteine che consentano di trasportarlo nel torrente ematico e “consegnarlo” ai tessuti che ne hanno bisogno. Queste proteine “da transito” si chiamano HDL, LDL, IDL, VLDL ed insieme al Colesterolo trasportano anche i Trigliceridi (i grassi che dovrebbero servire per l’energia). HDL (high-density-lipoprotein) lipoproteine ad alta densità. LDL (low-density-lipoprotein) lipoproteine a bassa densità.IDL (intermediate-density-lipoprotein) lipoproteine a densità intermedia.VLDL (very-low-density-lipoprotein) lipoproteine a bassisima densità.

3. Colesterolo buono e cattivoPerché si parla di “colesterolo LDL cattivo” e “colesterolo HDL buono”? LDL e HDL in realtà sono le proteine di trasporto cui è legato il colesterolo. Il ruolo delle HDL e delle LDLI trigliceridi e il colesterolo (rispettivamente, il carburante e la struttura) viaggiano insieme. Il viaggio parte dal fegato sulle VLDL. Mano a mano che le VLDL scaricano trigliceridi si alleggeriscono e diventano IDL. Successivamente le IDL, finito di scaricare trigliceridi alle varie cellule incaricate di immagazzinarli o di utilizzarli per produrre energia si trasformano in LDL ed iniziano a consegnare il colesterolo. Le HDL invece si occupano di ripulire i vasi dal colesterolo in eccesso e lo riportano al fegato per essere riciclato o per eliminarlo attraverso la bile. Le HDL sono a loro volta suddivise in 5 sotto classi, il cui ruolo esatto non è ancora chiaro, quello che si sa con certezza è che le HDL2 e le 3 assumono un ruolo importante e che la loro produzione è rispettivamente stimolata dall’esercizio e dal vino rosso.

4. Response of blood lipids to exercise training alone or combined with dietary intervention ARTHUR S. LEON, and OTTO A. SANCHEZ Med. Sci. Sports Exerc., Vol. 33, No. 6, Suppl., pp. S502–S515, 2001 Advances in the understanding of the role of blood lipids in atherosclerosis, cause of coronary heart disease (CHD), and related cardiovascular diseases. Specific questions that are addressed in this report : 1) Does the available evidence support the hypothesis that endurance exercise training has a favorable influence on the blood lipid profile relative to future risk of CHD? 2) Does the blood lipid responses to training differ by the study subjects’ sex, age, or race/ethnicity, and baseline lipid levels, and baseline relative body weight and its change with training? 3) Are the lipid responses to exercise related to the intensity, duration, the weekly volume of energy expenditure, the length of the endurance exercise program, and the associated changes with training in maximal oxygen uptake (V˙ O2max)?

5. The most frequently observed change is an increase in HDL-C, a protective factor against CHD (Evidence Category B). It is estimated that for every 0.026 mmol·L-1 (1 mg·dL-1) increase in HDL-C, the risk for a CHD event is reduced by 2% in men and at least 3% in women. Reduction in TC, LDL-C, and TG also may occur with training. In general, a 1% reduction in LDL-C is associated with a 2–3% lower risk of CHD. Exercise training also appears to attenuate the reduction in HDL-C accompanying a decreased dietary intake of saturated fat and cholesterol to promote reduction of LDL-C. Sex is not a predictor of responsiveness of HDL-C to training, with adult men and women appearing to respond similarly. Age also does not appear to be a predictor of lipid responsiveness to exercise training, with elderly men and women as likely, or perhaps even more likely, than younger individuals to increase HDL-C with training. There have been only a limited number of studies on the effects of different exercise intensities on blood lipids. Most of the studies used an exercise prescription involving moderate- to hard-intensity activities for at least 30 min, three times per week. There also is limited evidence that lower intensity (light-intensity) exercise may be as effective as moderate-intensity exercise in raising HDL-C.

6. Effects of exercise on glucose homeostasis in Type 2 diabetes mellitus DAVID E. KELLEY, and BRET H. GOODPASTER Med. Sci. Sports Exerc., Vol. 33, No. 6, Suppl., pp. S495–S501. The pathophysiology of Type 2 DM involves impaired insulin secretion, and impaired insulin action in regulating glucose and fatty acid metabolism in the liver, skeletal muscle, and adipose tissue. Many individuals with Type 2 DM have hypertension and perturbations of lipoprotein metabolism, as well as other manifestations of the insulin resistant syndrome. The purpose of this review is to examine data from randomized clinical trials, as well as other peer-reviewed research reports, to critically assess the therapeutic value of exercise in the management of Type 2 DM. Exercise appears to improve (decrease) the insulin resistance of peripheral tissues, and more specifically, to alleviate the defect of insulin-stimulated glycogen metabolism in skeletal muscle. Exercise was found to improve postprandial hyperglycemia, even if the effect on fasting hyperglycemia was minor. Exercise acutely lowers hepatic glucose production in Type 2 DM

7. The evidence from the prospective studies clearly suggests that an increase in physical activity prevents or at least delays the development of Type 2 DM in adults. It is clear from the available evidence that physical activity reduces the risk for development of Type 2 DM. Although the effects of exercise alone to improve glucose control in diabetes are not dramatic, the effects of physical activity on reducing cardiovascular risk factors in these patients are more obvious. Effects of exercise training on cardiovascular function and plasma lipid, lipoprotein, and apolipoprotein concentrations in premenopausal and postmenopausal women JA Blumenthal, K Matthews, M Fredrikson, N Rifai, S Schniebolk, D German, J Steege and J Rodin Arterioscler Thromb Vasc Biol 1991;11;912-917 Coronary heart disease risk is increased with high levels of total (TC) and low density lipoprotein (LDL-C) cholesterol and with low levels of high density lipoprotein cholesterol (HDL-C). Women have lower levels of LDL-C and higher levels of HDL-C than do their male counterparts

8. Cross-sectional studies have shown that postmenopausal women have higher TC, triglyceride, very low density lipoprotein cholesterol (VLDL-C), and LDL-C levels than do their premenopausal counterparts it is very difficult to attribute differences in lipid levels to the effects of exercise independent of hormonal status. Women can achieve significant improvements in aerobic capacity that are comparable to those in men; moreover, female hormones do not appear to affect the training response because premenopausal and postmenopausal women of comparable ages showed similar improvements in aerobic power. In general, aerobic endurance exercise for 3 months was generally not associated with improved lipid profiles.

9. EFFECTS OF THE AMOUNT AND INTENSITY OF EXERCISE ON PLASMA LIPOPROTEINS William E. K Raus , M.D., J Oseph A. H Oumard , P H .D., Brian D. Duscha , M.S., Kenneth J. Knetzger , M.S., Michelle B. Wharton , M.A., Jennifer S. Mc Cartney , M.A., Connie W. Bales , P H .D., R.D., Sarah Henes , R.D., Gregory P. Samsa , P H .D., James D. Otvos , P H .D., Krishnaji R. Kulkarni , P H .D., And Cris A. Slentz , P H .D. N Engl J Med, Vol. 347, No. 19 November 7, 2002 Increased physical activity is related to reduced risk of cardiovascular disease, possibly because it leads to improvement in the lipoprotein profile. However, the amount of exercise training required for optimal benefit is unknown. In a prospective, randomized study, we investigated the effects of the amount and intensity of exercise on lipoproteins. A total of 111 sedentary, overweight men and women with mild-to-moderate dyslipidemia were randomly assigned to participate for six months in a control group or for approximately eight months in one of three exercise groups: high-amount–high-intensity exercise, the caloric equivalent of jogging 20 mi (32.0 km) per week at 65 to 80 percent of peak oxygen consumption; low-amount–high- intensity exercise, the equivalent of jogging 12 mi (19.2 km) per week at 65 to 80 percent of peak oxygen consumption; or low amount–moderate-intensity exercise, the equivalent of walking 12 mi per week at 40 to 55 percent of peak oxygen consumption.

10. The optimal intensity or amount of exercise necessary for reductions in risk or risk factors is unknown. The data show a clear effect of the amount of exercise on lipoproteins and lipoprotein subfractions;they also show that a relatively high amount of regular exercise — even in the absence of clinically significant weight loss — can significantly improve the overall lipoprotein profile. These data refute the general conclusion, based on results from the standard lipid panel and on studies in which moderate amounts of exercise (similar to that in the low-amount groups in our study) were used, that exercise has only limited effects on lipids and lipoproteins. The second major finding is that the amount of exercise appears to make a greater difference than the intensity of exercise on plasma lipoprotein concentrations. Our data, taken together with those of others, suggest that any effect on lipids of the intensity of exercise is small as compared with that of the amount of exercise. Although the lower amount of exercise resulted in fewer significant improvements, this amount of exercise was able to limit or prevent in the low-amount groups much of the weight gain and consequent worsening of the overall lipoprotein profile that was observed in the control group

11. Although the two high intensity groups had very similar increases in fitness (as measured by peak oxygen consumption), only the high-amount group had extensive improvements in the overall lipoprotein profile. Similarly, the same low amount of weekly exercise had very different effects on fitness in the high-intensity group and the moderate-intensity group but had similar effects on the lipoprotein profile in the two groups. Therefore, it would appear that it is the amount of activity — and not necessarily the change in fitness — that is important for the improvement of the lipoprotein profile with exercise programs.