Goszka G, Brymora A, Flisiński M, i wsp. Występowanie i wpływ spożycia fruktozy na przemiany metaboliczne oraz jej potencjalne ryzyko wzrostu powikłań chorób metabolicznych. Med Biol Sci 2010; 24(2): 11–15.
Schleip T. Fruktoza. Brak tolerancji na cukier owocowy. Warszawa: Oficyna Wydawnicza „Interspar”; 2006: 58–76.
Jermendy G. Intensive insulin therapy in type 2 diabetes mellitus. Diabet Care 2012; 23, 153(38): 1487–1493.
Busserolles J, Gueux E, Rock E. Oligofructose protects against the hypertrigliceridemic and prooxidative effects of a high fructose diet in rats. J Nut 2003; 133: 1903–190
Busserolles J, Gueux E, Rock E, et al. Substituting honey for refined carbohydrates protects rats from hypertriglyceridemic and prooxidative effects of fructose. J Nutr 2002; 132: 3379–3382.
Lee SJ, Terkeltaub RA, Kavanaugh A. Recent developments in diet and gout. Curr Opin Rheumatol 2006; 18: 193–198.
Bogdanov S, Jurendic T, Sieber R, et al. Honey for nutrition and heath: a review. Am J College Nutr 2008; 27: 677–689.
Johnson RJ, Perez-Pozo SE , Sautin YY , et al. Hypothesis: could excessive fructose intake and uric acid cause type 2 diabetes?Endocr Rev 2009; 30: 96–116.
Tsioufis C, Chatzis D, Vezali E, et al. The controversial role of serum uric acid in essentials hypertension: relationships with indices of target organ damage. J Hum Hypertens 2005; 19: 211–217.
Johnson RJ, Kivlighn SD, Kim Y-G, et al. Reappraisal of the pathogenesis and consequences of hyperurycemia in hypertension,cardiovascular disease, and renal Disease. AJKD 1999; 33(2): 225–234.
Arnold B, Alper Wei Chen Jr, et al. Childhood uric acid predicts adult blood pressure: the Bogalusa Heart Study. Hypertension 2005; 45: 34–38
Feig D, Nakagawa T, Karumanchi SA , et al. Uric acid, nephron number and the pahogenesis of essential hypertension. Kidney Int 2004; 66: 281–287.
Tykarski A. Ocena transportu kwasu moczowego w nefronie w nadciśnieniu tętniczym pierwotnym. Pol Arch Med Wewn 1991; 86: 167–176.
Kostka-Jeziorny K, Uruski P, Tykarski A. Wpływ allopurinolu na prędkość fali tętna u pacjentów z nadciśnieniem tętniczym w zależności od stosowanej terapii hipotensyjnej. Nadciśn Tętn 2009; 13(4): 246–257.
Jastrzębski M, Klocek M, Czarnecka D, i wsp. Kwas moczowy u chorych na pierwotne nadciśnienie tętnicze – zależności kliniczne i biochemiczne. Nadciśn Tętn 2008; 12(5): 352–358.
Leyva F, Anker SD, Godsland IF, et al. Uric acid in chronic heart failure: a marker of chronic inflammation. Eur Heart J 1998;19: 1814–1822.
Kostka-Jeziorny K, Tykarski A. Wpływ terapii hipotensyjnej na stężenie kwasu moczowego. Nadciśn Tętn 2007; 11(2): 151––163
Reyes A. The increase in serum uric acid concentration caused by diuretics might be beneficial in heart failure. Eur J Heart Fail 2005; 7: 461–467.
Kostka-Jeziorny K, Tykarski A. Losartan, allopurinol – czy są dowody, że hiperurykemia może stać się kolejnym celem terapii w prewencji ryzyka sercowo-naczyniowego u pacjentów z nadciśnieniem tętniczym. Nadciśn Tętn 2009; 13(4): 219–238.
Kramer CK , von Mühlen D, Jassal SK , et al. Serum uric acid levels improve prediction of incident type 2 diabetes in individuals with impaired fasting glucose: the Rancho Bernardo Study. Diabet Care 2009; 32(7): 1272–1273.
Ben-Dovi I, Kark J. Serum uric acid is a GFR-independent long-term predictor of acute and chronic renal insufficiency: the Jerusalem Lipid Research Clinic Cohort Study. Nephrol Dial Transplant 2011; 26(8): 2558–2566.
Glushakova O, Kosugi T, Johnson RJ, et al. Fructose induces the inflammatory molecule ICA M-1 in endothelial cell. J Am Soc Nephrol 2008; 19: 1712–1720.
Cirillo P, Gersch MS, Johnson RJ, et al. Ketohexokinase – dependent metabolism of fructose induces proinflamatory mediators in proximal tubular cell. J Am Soc Nephrol 2009; 20: 545–553.
Gersch MS, Mu W, Cirillo P, et al. Fructose, but not dextrose, accelerates the progression of chronic kidney disease. Am J Physiol Renal Physiol 2007; 293: F1256–F126
Johnson RJ, Segal MS, Sautin Y, et al. Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease. Am J Clin Nutr 2007; 86(4): 899–906.
Feig D, Kang DH, Johnson RJ. Uric acid and cardiovascular risk. N Engl J Med 2008; 359(17): 1811–1821.
Chen Sz, Chang JM, Yeh SM, et al. Association of uric acid and left ventricular mass index with renal outcomes in chronic kidney disease. Am J Hypertens 2012. doi: 10.1093/ajh/hps020 First published online: December 28, 2012.
Tamariz L, Agarwal S, Soliman EZ , et al. Association of serum uric acid with incident atrial fibrillation (from the Atherosclerosis Risk in Communities [ARIC] Study). Am J Cardiol 2011; 108(9): 1272–1276.
Young Kim S, Guevara JP, Kim KM, et al. Hyperuricemia and risk of stroke: a systematic review and meta-analysis. Arthritis Rheum 2009; 15, 61(7): 885–892.
Noh H-L, Hu Y, Park T-S, et al. Regulation of plasma fructose and mortality in mice by the aldose reductase inhibitor lidorestat.J Pharmacol Exp Ther 2009; 328: 496–503.
Meller KM, Bell JR, Wendt IR, et al. Fructose modulates cardiomyocyte excitation-contraction coupling and Ca2+ handling in vitro. PLoS ONE 2011; 6: e-25204–e 252010.
Douard V, Rerrris RP. Regulation of the fructose transporter GLU T5 in health and disease. Am J Physiol Endocrinol Metab 2008; 295: E227–E237.
Chess DJ, Xu W, Khairallah R, et al. The antioxidant tempol attenuates pressure overload-induced cardiac hypertrophy and contractile dysfunction in mice fed a high-fructose diet. Am J Physiol Heart Circ Physiol 2008; 295: H2223–H2230.
Mellor K, Ritchie RH, Meredith G, et al. High-fructose diet elevates myocardial superoxide generation in mice in the absence of cardiac hypertrophy. Nutrition 2010; 26: 842–848.
Fang Y-Z, Sheng Y, Wu G. Free radicals, antioxidants, and nutrition. Nutrition 2002; 18: 872–879.
Shinozaki K, Ayajiki K, Nishio Y, et al. Evidence for a causal role of the rennin–angiotensin system in vascular dysfunction associated with insulin resistance. Hypertension 2004; 43: 255–262.
Delbosc S, Paizanis E, Maqous R. Involvement of oxidative stress and NA DPH oxidase activation in the development of cardiovascular complications in a model of insulin resistance, the fructose-fed rat. Atherosclerosis 2005; 179: 43–49.
Nagail Y, Ichihara A, Nakano D, et al. Possible contribution of the non-proteolytic activation of prorenin to the development of insulin resistance in fructose-fed rats. Exp Physiol 2009; 94: 1016–1023.
Sautin YY , Nakagawa T, Zharikov S, et al. Adverse effects of the classic antioxidant uric acid in adipocytes: NA DPH oxidase-mediated oxidative/nitrosative stress. Am J Physiol Cell Physiol 2007; 293: C584–C596.
Kawasaki T, Akanuma H, Yamanouchi T. Increased fructose concentrations in blood and urine in patients with diabetes. Diabet Care 2002; 25: 353–357.
Reiser S, Smith C, Mertz W, et al. Indices of copper status in humans consuming a typical American diet containing either fructose or starch. Am J Clin Nutr 1985; 42: 242–251