Hai cercato la traduzione di diffuse fatty liver changes da Inglese a Arabo

fatty liver
كَبِدٌ دُهْنِيَّة

nonalcoholic fatty liver disease
مرض الكبد الدهني غير الكحولي

diagnosis of alcoholic fatty liver
تشخيص الكبد الدهني الكحولي

we can confirm fatty liver with an ultrasound.
يمكننا التأكد من مرض الكبد السمين بلتصوير بالصدى

and his fatty liver indicates a lot of drinking.
وكبده الدهنية تشير إلى الكثير من الشرب.

what causes nonalcoholic fatty liver disease (nash)?
the cause of nonalcoholic fatty liver disease is complex and not completely understood.

fatty liver with sparing areas no focal mass lesion
مجانية على الانترنت القاموس الطبي engilsh إلى الفارسية

acute fatty liver of pregnancy would have the same symptoms.
الدهن الحاد للكبد بالحمل لديه نفس الأعراض

today, 33% of americans have a fatty liver, which causes chronic metabolic disease.
*** untranslated ***

nonalcoholic fatty liver disease nonalcoholic fatty liver disease is a manifestation of an abnormality of metabolism within the liver
مرض الكبد الدهني غير الكحولي مرض الكبد الدهني غير الكحولي هو مظهر من مظاهر شذوذ التمثيل الغذائي داخل الكبد

obesity s/p roux en y gastric bypass cirrhosis secondary to fatty liver disease and chronic hepatitis b infection chronic abdominal pain
تَفاغُرٌ مِعَوِيٌّ بشَكْلِ y لمعالجة البدانة تشمع الكبد الثانوي لداء تشحم الكبد و التهاب الكبد b الإنتاني المزمن ألم بطني مزمن

so this is very nonspecific, but it means the liver is sick, and the most likely cause of your liver sickness is a fatty liver.
وهذا لم يحدث مما يعني أن البنكرياس مريض وهذا بسبب دهون موجودة عليه

acute and chronic viral hepatitis (a, b,c), autoimmune hepatitis, fatty liver, cirrhosis, and other liver disorders
الالتهاب الكبدي الفيروسي الحاد والمزمن (أ، ب، جـ)، والالتهاب الكبدي بالمناعة الذاتية، والكبد الدهني، والتليف الكبدي، وغير ذلك من اضطرابات الكبد

nonalcoholic fatty liver disease chronic hepatitis b infection cirrhosis of the liver - likely secondary to both of the above h pylori infection
مرض الكبد الدهني غير الكحولي الالتهاب الكبدي الفيروسي المزمن b تشمّع الكبد - من المحتمل أن يكون ثانوياً للأمراض المذكورة أعلاه إنتان بجرثومة الحلزونية البوّابية

nonalcoholic fatty liver disease is classified as either fatty liver (sometimes referred to as isolated fatty liver or ifl) or steatohepatitis (nash).
يصنف مرض الكبد الدهني غير الكحولي إما على أنه كبد دهني (يشار إليه أحيانًا باسم الكبد الدهني المعزول أو ifl) أو التهاب الكبد الدهني (nash).

and in fact, this molecule prevents this adipocyte, this fat stem cell, from remembering how to make fat such that mice on a high fat diet, like the folks in my hometown of chicago, fail to develop fatty liver, which is a major medical problem.
وفي الواقع، فإن هذا الجزئ يمنع هذه الخلية الشحمية، هذه الخلية الجذعية الدهنية، من تذكر كيفية صنع الدهون بحيث أن الفئران التي تتناول أغذية مشبعة بالدهون، مثل الناس في مدينتي شيكاغو، لا يمكن لكبدها أن تصبح دهنية، مما يمثل معضلةً طبية كبرى.

however, there were no liver changes at 50 mg/kg diet (noael 50 mg/kg, loael 100 mg/kg diet) (fitzhugh et al., 1950).
ولكن لم تحدث أي تغيّرات في الكبد عند جرعة بمقدار 50 م غ/ك غ في الغذاء (مستوى انعدام الأثر الضار المُلاحَظ (noael) 50 م غ/ك غ، وأدنى مستوى للأثر الضار المُلاحظ (loael) 100 م غ/ك غ في الغذاء) (fitzhugh et al., 1950).

in both isolated fatty liver and nash there is an abnormal amount of fat in the liver cells, but, in addition, in nash there is inflammation within the liver, and, as a result, the liver cells are damaged, die, and are replaced by scar tissue.
في كل من الكبد الدهني المعزول وناش هناك كمية غير طبيعية من الدهون في خلايا الكبد ، ولكن ، بالإضافة إلى ذلك ، في ناش هناك التهاب داخل الكبد ، ونتيجة لذلك ، تتلف خلايا الكبد ، وتموت ، ويتم استبدالها بأنسجة الندبات.

there is another form of fatty liver, termed nonalcoholic fatty liver disease (nonalcoholic fatty liver disease), in which alcohol has been excluded as a cause. in nonalcoholic fatty liver disease, other recognized causes of fatty liver that are less common causes than alcohol also are excluded.
هناك شكل آخر من أشكال الكبد الدهني ، يسمى مرض الكبد الدهني غير الكحولي (مرض الكبد الدهني غير الكحولي) ، حيث تم استبعاد الكحول كسبب. في مرض الكبد الدهني غير الكحولي ، يتم أيضًا استبعاد الأسباب الأخرى المعروفة للكبد الدهني الأقل شيوعًا من الكحول.

metabolic variables and basal substrate kinetics basal glucose and fatty acid kinetics. basal glucose and palmitate kinetics were not different between matched subjects within any of the 2 groups (table 2). insulin sensitivity. hepatic (fig. 1a), skeletal muscle (fig. 1b), and adipose tissue (fig. 1c) insulin sensitivity was lower in subjects with high than in those with normal ihtg content. however, no differences in insulin sensitivity measures were observed between subjects with low or high vat volume, when matched on ihtg content (fig. 1). fig. 1. fig. 1. hepatic (a), skeletal muscle (b), and adipose tissue (c) insulin sensitivity in subjects matched on visceral adipose tissue (vat) volume with either normal or high intrahepatic triglyceride (ihtg) content and subjects matched on ihtg content who had either ... vldl-tg kinetics. hepatic vldl-tg secretion rate was almost double in subjects with high than in those with normal ihtg content (23 ± 2 and 12 ± 1 μmol/min, respectively; p 10% of liver volume) (n = 10) or normal (≤5.5% of liver volume) (n = 10) ihtg content (table 1) (41). the range in vat volume was similar in both the normal (vat volume: 689–3,088 cm3) and the high (vat volume: 638–2,702 cm3) ihtg groups. each subject with normal ihtg and a given vat volume was matched with a subject from the high ihtg group on vat (within ≈20% of vat volume of the normal ihtg group). group 2 subjects (n = 20) were matched on ihtg content and had either low (n = 10) or high (n = 10) vat volume (table 1). subjects were separated into low and high vat volume groups by using the median value of all subjects (1,100 cm3) as the cut point for low and high vat volumes. subjects within groups were matched on age, sex, bmi, and percentage of body fat. we did not have knowledge of any outcome measures when the matches were performed. all subjects completed a comprehensive medical evaluation, which included a 2-h oral glucose tolerance test. no subject had any history or evidence of liver disease other than nafld, took medications that can affect metabolism or cause hepatic abnormalities, consumed >20 g/day of alcohol, or had diabetes. subjects gave their written informed consent before participating in this study, which was approved by the human research protection office of washington university school of medicine, st. louis, mo. body composition analyses. body fat mass (fm) and fat-free mass (ffm) were determined by using dual-energy x-ray absorptiometry (delphi-w densitometer, hologic). intraabdominal and abdominal s.c. adipose tissue volumes were quantified by magnetic resonance imaging (siemens; analyze 7.0 software, mayo foundation) (9) and ihtg content was measured by using proton magnetic resonance spectroscopy (siemens) as we have previously described (42). hyperinsulinemic–euglycemic clamp procedure. subjects were admitted to the intensive research unit at washington university school of medicine on the evening before the clamp procedure. at 0500 hours the following morning, after subjects fasted for 12 h overnight, a 2-stage hyperinsulinemic–euglycemic clamp procedure was started and continued for 9 h. insulin was infused at a rate of 20 mu·m−2 body-surface area (bsa)·min−1 during stage 1 (3–6 h) and at a rate of 50 mu·m−2 bsa·min−1 during stage 2 (6–9 h) of the clamp procedure (9, 43). [6,6-2h2]glucose, [2,2-2h2]palmitate, and 20% dextrose enriched to 2.5% with [6,6-2h2]glucose were infused to determine hepatic, skeletal muscle, and adipose tissue insulin sensitivity. tissue samples were obtained from s.c. abdominal adipose tissue and from the quadriceps femoris muscle 60 min after starting the glucose tracer infusion during the basal stage. a detailed description of the infusion protocol and of collection of tissues and blood samples is available in supporting information (si) materials and methods. vldl-tg kinetics study. one week after the hyperinsulinemic–euglycemic clamp procedure, subjects were readmitted to the intensive research unit on the evening before the vldl kinetics study. at 0600 hours the following morning, after subjects fasted for 12 h overnight, a bolus of [1,1,2,3,3-2h5]glycerol was injected, and a constant infusion of 2,2-2h2]palmitate was started and main
metabolic variables and basal substrate kinetics basal glucose and fatty acid kinetics. basal glucose and palmitate kinetics were not different between matched subjects within any of the 2 groups (table 2). insulin sensitivity. hepatic (fig. 1a), skeletal muscle (fig. 1b), and adipose tissue (fig. 1c) insulin sensitivity was lower in subjects with high than in those with normal ihtg content. however, no differences in insulin sensitivity measures were observed between subjects with low or high vat volume, when matched on ihtg content (fig. 1). fig. 1. fig. 1. hepatic (a), skeletal muscle (b), and adipose tissue (c) insulin sensitivity in subjects matched on visceral adipose tissue (vat) volume with either normal or high intrahepatic triglyceride (ihtg) content and subjects matched on ihtg content who had either ... vldl-tg kinetics. hepatic vldl-tg secretion rate was almost double in subjects with high than in those with normal ihtg content (23 ± 2 and 12 ± 1 μmol/min, respectively; p 10% of liver volume) (n = 10) or normal (≤5.5% of liver volume) (n = 10) ihtg content (table 1) (41). the range in vat volume was similar in both the normal (vat volume: 689–3,088 cm3) and the high (vat volume: 638–2,702 cm3) ihtg groups. each subject with normal ihtg and a given vat volume was matched with a subject from the high ihtg group on vat (within ≈20% of vat volume of the normal ihtg group). group 2 subjects (n = 20) were matched on ihtg content and had either low (n = 10) or high (n = 10) vat volume (table 1). subjects were separated into low and high vat volume groups by using the median value of all subjects (1,100 cm3) as the cut point for low and high vat volumes. subjects within groups were matched on age, sex, bmi, and percentage of body fat. we did not have knowledge of any outcome measures when the matches were performed. all subjects completed a comprehensive medical evaluation, which included a 2-h oral glucose tolerance test. no subject had any history or evidence of liver disease other than nafld, took medications that can affect metabolism or cause hepatic abnormalities, consumed >20 g/day of alcohol, or had diabetes. subjects gave their written informed consent before participating in this study, which was approved by the human research protection office of washington university school of medicine, st. louis, mo. body composition analyses. body fat mass (fm) and fat-free mass (ffm) were determined by using dual-energy x-ray absorptiometry (delphi-w densitometer, hologic). intraabdominal and abdominal s.c. adipose tissue volumes were quantified by magnetic resonance imaging (siemens; analyze 7.0 software, mayo foundation) (9) and ihtg content was measured by using proton magnetic resonance spectroscopy (siemens) as we have previously described (42). hyperinsulinemic–euglycemic clamp procedure. subjects were admitted to the intensive research unit at washington university school of medicine on the evening before the clamp procedure. at 0500 hours the following morning, after subjects fasted for 12 h overnight, a 2-stage hyperinsulinemic–euglycemic clamp procedure was started and continued for 9 h. insulin was infused at a rate of 20 mu·m−2 body-surface area (bsa)·min−1 during stage 1 (3–6 h) and at a rate of 50 mu·m−2 bsa·min−1 during stage 2 (6–9 h) of the clamp procedure (9, 43). [6,6-2h2]glucose, [2,2-2h2]palmitate, and 20% dextrose enriched to 2.5% with [6,6-2h2]glucose were infused to determine hepatic, skeletal muscle, and adipose tissue insulin sensitivity. tissue samples were obtained from s.c. abdominal adipose tissue and from the quadriceps femoris muscle 60 min after starting the glucose tracer infusion during the basal stage. a detailed description of the infusion protocol and of collection of tissues and blood samples is available in supporting information (si) materials and methods. vldl-tg kinetics study. one week after the hyperinsulinemic–euglycemic clamp procedure, subjects were readmitted to the intensive research unit on the evening before the vldl kinetics study. at 0600 hours the following morning, after subjects fasted for 12 h overnight, a bolus of [1,1,2,3,3-2h5]glycerol was injected, and a constant infusion of 2,2-2h2]palmitate was started and main