Tabi google çeviri kabul etmiyorsunuz sanırım 1 saat uğraşıp çevirmem gerekiyordu. translate çevirisi atmadım ayrıca
. çok iyi niyetliyseniz siz yazdıklarınızı çevirseydiniz akademik ingilizce bilmeyenlerde yararlansaydı. yaptığım çeviride ise bir yanlışlık yok sanki konuyu kendi lehime çevirip atmışım gibi tepki vermeyin lütfen. neyse konumuza dönelim;
There is no doubt that high-fructose feeding can cause several adverse effects (Table 1), because fructose stimulates DNL more than other carbohydrate sources.
Table 1'de ise bir çok hayvan ve insanlar üstünde yapılan bir araştırmanın sonuçlarından yola çıkarak hazırlanılmış. Bizi ilgilendiren kısmı ise yüksek fruktoz alımlarında;
Human 15 5 wk ↑ Insulin concentrations (14%) in hyperinsulinemic and glucose-intolerant subjects (235%) Hallfrisch et al.
20 5 wk ↑ TG (47%) in hyperinsulinemic and (20%) nonhyperinsulinemic subjects Reiser et al.
İkinci çalışmamıza bakalım;
Dietary fructose is a major contributor to insulin resistance and metabolic syndrome, disturbing tissue and organ functions. Fructose is mainly absorbed into systemic circulation by glucose transporter 2 (GLUT2) and GLUT5, and metabolized in liver to produce glucose, lactate, triglyceride (TG), free fatty acid (FFA), uric acid (UA) and methylglyoxal (MG). Its extrahepatic absorption and metabolism also take place. High levels of these metabolites are the direct dangerous factors. During fructose metabolism, ATP depletion occurs and induces oxidative stress and inflammatory response, disturbing functions of local tissues and organs to overproduce inflammatory cytokine, adiponectin, leptin and endotoxin, which act as indirect dangerous factors. Fructose and its metabolites directly and/or indirectly cause oxidative stress, chronic inflammation, endothelial dysfunction, autophagy and increased intestinal permeability, and then further aggravate the metabolic syndrome with tissue and organ dysfunctions. Therefore, this review addresses fructose-induced metabolic syndrome, and the disturbance effects of direct and/or indirect dangerous factors on the functions of liver, adipose, pancreas islet, skeletal muscle, kidney, heart, brain and small intestine. It is important to find the potential correlations between direct and/or indirect risk factors and healthy problems under excess dietary fructose consumption.
Aynı çalışmanın devamında ise fruktozun gereksiz fazla alınması ile doğabilecek metabolik sendromlardan bahsetmekte ve bir tabloda bunu açıklamaktadır.
Fructose is widely found in natural foods, including fruits, vegetables and honeys, and is added to commercial food additives. Overconsumption of fructose is a risk factor for the epidemic of metabolic syndrome (MetS), with dysfunctions in multiple tissues and organs including liver, adipose, pancreatic islet, skeletal muscle, kidney, heart, brain and intestine. The primary metabolites from fructolysis are produced in liver and secreted into system circulation, directly affecting tissue and organ functions; among these free fatty acids (FFA), uric acid (UA) and lactate play central roles in inducing insulin resistance in systemic and local tissue and organ, as well as causing reactive oxygen species (ROS) overproduction. These dysfunction events consequently lead to secretion of indirect dangerous factors, such as inflammatory cytokine, adiponectin, leptin and endotoxin. These indirect adverse factors give rise to inflammatory response, lipid accumulation, and endothelial dysfunction in local tissues and organs, in addition to the appetite disturbance for food intake, further aggravating the metabolic burden of fructose (summarized in
Figure 1). Discussion of these direct and indirect adverse molecules in circulation helps us to uncover the clues for tissue and organ function disturbance and their correlation (
Table 1). These adverse effects of high fructose consumption remind us to be cautious about excess fructose intake in our daily diet. More importantly, relevant government departments should make policies about the quality standard and safety of food additives to improve supervisions.
Bir diğer farklı çalışmamızda ise uzun süreli yüksek fruktoz alımının tip2 diyabete varan rahatsızlıklarla sonuçlanabileceğini görüyoruz;
On the other hand, observations from numerous mechanistic studies in cells, animals, healthy volunteers, and patients clearly demonstrate that fructose has lipogenic potential. Hepatic fructose metabolism rapidly produces gluconeogenesis and lipogenesis precursors, while intermediary fructose metabolites also act as nutritional regulators of the major transcription factors that control these pathways. Accordingly, fructose ingestion increases plasma triglyceride levels and high-fructose diets promote hepatic DNL [
46,
54,
55]. Hepatic DNL is an important contributor to intrahepatic lipids in human NAFLD, suggesting that long-term fructose overconsumption may promote mechanisms that drive NAFLD development. Moreover, the overall evidence linking increased fructose intake to hepatic insulin resistance, increased uric acid concentrations, and NAFLD severity/progression is more convincing.
Finally, we are confident that a deeper understanding of the cellular mechanisms governing hepatic fructose metabolism will reveal novel targets for NAFLD/NASH, hypertriglyceridemia, and hepatic insulin resistance/type 2 diabetes.
Eki Görüntüle 50782
Bambaşka bir araştırmada ise yüksek fruktoz tüketiminin vücut yağına rahatlıkla dönüşebildiği saptanmış.
In comparison to calorically-equivalent consumption of diets containing glucose, prolonged consumption of diets containing fructose (11 weeks) increased BW and body fat deposition. Similarly, Bremer et al.
50, found that healthy middle-aged rhesus macaques experienced significant increases in BW and adiposity when fed 30% daily energy intake from fructose for 1 year despite minimal changes in calorie intake (3%). These results are also similar to animal studies in which increases in fat deposition and liver mass were observed when rodents were fed fructose compared with other purified monosaccharides; however such interventions were unmatched for calorie intake
51,
52. Furthermore, studies in humans confirm that fructose, but not glucose (when provided as 25% of energy requirements), in the context of an energy-balanced diet increases
de novo lipogenesis and visceral adiposity along with dyslipidemia, decreases insulin sensitivity
10,
12 and decreases in fat oxidation
53. Curiously, in human studies that use isocaloric diets with subjects in energy balance (i.e., equal energy intake and expenditure), observed no overall effects of fructose in BW gain
20,
21. However, it is worth mentioning that such interventions in humans tend to be of very short duration (up to 4 weeks), so it is not clear whether such null effects on BW will persist in longer term interventions. In the present study, we addressed this question by using a more prolonged intervention (11 weeks) which allowed us to assess the long-term effects of fructose intake. This is also more relevant for humans since the ultimate goal is to clarify the role of fructose consumption in the obesity epidemic.
5 dakikada bulduğum ve sadece pubmedten bile kolayca bulunabilecek araştırmalar bunlar. nasıl denk gelmedin daha önce bilmiyorum artık
yüzlercesi daha var tartışmak yerine girip kendin okuyabilirsin zaten.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4403227/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5409674/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5622741/
Ayrıyetten fruktoz benim kan davalımmış gibi gözüküyor bu konuda. Lakin hala kendimi anlatamadığımı düşünüyorum.
Ben meyve düşmanı biri değilim ve meyve sağlıksızdır demiyorum. Elbetteki kalori açığı devam ederken 1 adet yeşil elma sizi obez yapmaz, yapamaz.
Benim anlatmak istediğim
sıkı bir diyet uygulayacak ve bir an önce hedefinize varacaksanız gereksiz şeker alımı yapmayın demek!
Bu mantıkla ilerlersek günde 15gr zeytinyağıda sizi yağlandırmaz ancak hedefinizden uzaklaştırır. Ben böyle dediğim için zeytinyağı zararlı mı? Günlük makroların çerçevesinde yağınıda, karbonhidratınıda tüket tabi ki!. Ancak günlük alman gereken şeker 50gr ise ve sen fruktozda olsa 100gr alıyorsan ve yulafından, pirincinden kısıyorsan bu seni hedefinden uzaklaştırır. Gayet mantık çerçevesinde anlattığımı düşünüyorum artık kendimi. Lütfen bana meyve sağlıksızdır diyeni keserim ulan diyerek gelmeyin artık. Benim öyle bir iddiam yok. Yukarıda ise meyve sağlıksızdır diyen araştrmaları değil, yüksek fruktoz alımının arkadaşların anlattığı gibi masum olmadığını gösteren araştırmalar koydum. Lütfen böyle bilin ve sağlıcakla kalın! İyi geceler.
--- Mesaj birleştirildi, 11 Eylül 2018 ---
Ayrıyetten attığınız çalışmalar günlük kalori limitinin içinde yapılan fruktoz alımlarını gösteriyor. Bunu belirtmeyi unutmuşum. Benim anlatmaya çalıştığım şey ise 2000 olan kalori ihtiyacının tamamını aldın ve oturdun 250 kalorilik meyve yedin diyelim. Bu 250 kalorilik meyve seni yağlandırı yani bunu hepimiz biliyoruz zaten?????
Genişletmek için tıkla...