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Results for intrahepatic colangiocarcinoma translation from English to Arabic

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English

intrahepatic

Arabic

الاقنية, داخل الكبد (علم التشريح)

Last Update: 2018-04-14
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intrahepatic

Arabic

داخل الكبد

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intrahepatic

Arabic

داخِلَ الكَبِد

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intrahepatic cholangiojejunostomy

Arabic

مُفاغَرةٌ صَفْراوِيَّةٌ صائِمِيَّةٌ داخِلَ الكَبِد

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intrahepatic cholestasis

Arabic

رُكودٌ صَفْراوِيٌّ داخِلَ الكَبِد

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intrahepatic cholangitis

Arabic

الْتِهابُ الأَقْنِيَةِ الصَّفْراوِيَّةِ داخِلَ الكَبِد

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intrahepatic bile duct adenoma

Arabic

الوَرَمُ الغُدِّيُّ فِي الأقنية الصِّفْراوية داخِلَ الكَبِدِيَّة

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No intrahepatic biliary duct dilatation.

Arabic

لا يوجد توسع في القُنَيَّات الصَّفْراوِيَّة داخل الكبد.

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No intrahepatic biliary radicles dilatation.

Arabic

لا يوجد توسع في الجُذَيرات داخل الكبد.

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Diagnosis of malignant neoplasm on the intrahepatic bile duct carcinoma

Arabic

تشخيص الأورام الخبيثه على سرطان القنوات المراريه داخل الكبد

Last Update: 2018-07-23
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On ultrasound, we found intrahepatic dilated bile ducts.

Arabic

وجدنا بفحص الموجات قنوات مراريّة متمدّدة داخل الكبد

Last Update: 2016-10-27
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Diagnosis of secondary malignant neoplasm of liver and intrahepatic bile duct

Arabic

تشخيص أورام ثانويه خبيثة بالكبد والقناة الصفراوية داخل الكبد

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Intrahepatic branches of hepatic arterial system seems to course through this ill defined hypodense area.

Arabic

يبدو أن الفروع داخل الكبد للجملة الشريانية الكبدية تمر عبر هذه المنطقة ناقصة الكثافة غير المحددة

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The liver showed no focal lesion but intrahepatic pneumobilia and evidence of gas shadow in the CBD shown.

Arabic

لم يظهر الكبد أي آفة بؤرية ولكنه أظهر استرواح الجهاز الصفراوي داخل الكبد وهو ما يدل على وجود الظل الغازي في القناة المرارية المشتركة.

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The sheer complexity of biological systems means that any effort to understand insulin resistance with a unified, succinct, and straightforward model may be a fool’s errand. Certainly normal insulin action, despite sharing important effectors among different cell types, performs myriad functions that are not particularly amenable to encapsulation. In particular, understanding the intricate relationship between insulin control of both lipid and carbohydrate metabolism has proved a worthy challenge for generations of investigators (532). But in considering the several putative mediators of insulin resistance discussed in the preceding sections, it is tempting both to note potential areas of unification and to veer into teleological speculation. The fundamental element linking all putative mediators of insulin resistance is a relationship to nutrient oversupply. Each mechanism discussed in this review is proposed to cause insulin resistance by either increasing nutrient-derived toxic metabolites (DAG, ceramide, acylcarnitine, BCAA), overdriving nutrient utilization processes (ER stress, oxidative stress), or responding to nutrient stressmediated cellular toxicity (inflammation). Moreover, the pathophysiology of insulin resistance driven by cellular stress pathways and by inflammation shares common threads with the insulin resistance induced by bioactive lipids. ER stress promotes de novo lipogenesis. The mitochondrial dysfunction of aged and insulin-resistant humans facilitates positive energy balance and ectopic lipid storage. Adipose tissue inflammation drives lipolysis, increasing substrate delivery to nonadipose tissues. We therefore propose an integrated model of insulin resistance in which several simultaneous responses to nutrient oversupply converge and collide to facilitate ectopic lipid accumulation and consequent insulin resistance in skeletal muscle and liver (FIGURE 19). If overnutrition is the central driver of all these metabolic defects, then the most obvious therapeutic option is calorie restriction. Although the cellular effects of caloric restriction are complex and incompletely understood, the physiological effects of applying a hypocaloric diet to an obese insulin-resistant subject represent a useful test of the hypotheses presented in this review. Recently, Perry et al. (625) catalogued the metabolic consequences of a 3-day very-low-calorie diet (VLCD; 25% of normal caloric intake) in a rat model of insulin-resistant T2D (4 wk of high-fat feeding or Western diet followed by low-dose streptozotocin/nicotinamide to achieve fasting hyperglycemia). Without significantly reducing body weight, VLCD achieved near-normalization of plasma glucose and insulin levels. This was associated with reductions in IHTG, hepatic acetyl CoA, hepatic membrane-associated DAG, and hepatic PKC activation; parameters that did not change included hepatic ceramides, plasma glucagon, a panel of inflammatory cytokines, plasma FGF21, plasma BCAAs, and hepatic ER stress markers (625). In hyperinsulinemic-euglycemic clamp studies, VLCD resulted in increased AKT activation and insulin suppression of HGP (625). Interestingly, both direct and indirect components of hepatic insulin action were improved by VLCD; the improvements in HGP seen with VLCD could be abrogated by acetate infusion (to prevent VLCD-induced decreases in hepatic acetyl CoA) or recapitulated by a glycogen phosphorylase inhibitor (to simulate VLCD-induced improvements in insulin-stimulated hepatic glycogen synthesis) (625). The utility of this rapid intervention is that it helps to distinguish the parameters that drive hyperglycemia from those that are secondary consequences or exacerbating factors. The results incriminate hepatic DAG-PKC axis activation and metabolite-driven gluconeogenesis. Yet all studies have limitations, and a major limitation of the above study is one shared by much of the work cited in this review: the use of a rodent model to draw inferences about human pathophysiology. One of the rodent-human differences most germane to the study of insulin resistance is the order in which tissues develop insulin resistance upon overnutrition. In rodents, just a few days of high-fat feeding is sufficient to cause hepatic steatosis and hepatic insulin resistance; skeletal muscle insulin resistance requires several weeks to develop (429). In those weeks, meanwhile, WAT expands and eventually becomes inflamed, stimulating liINSULIN ACTION AND INSULIN RESISTANCE Physiol Rev • VOL 98 • OCTOBER 2018 • www.prv.org 2193 Downloaded from journals.physiology.org/journal/physrev (041.232.128.179) on April 13, 2021. polysis and in turn hepatic gluconeogenesis (620). In humans, available evidence points to skeletal muscle insulin resistance as the first defect; the young, healthy, lean offspring of type 2 diabetics display skeletal muscle insulin resistance but normal IHTG and normal hepatic insulin action (639). Muscle insulin resistance promotes hepatic lipogenesis, however, and eventually NAFLD and hepatic insulin resistance develop. How adipose insulin resistance fits into this paradigm in humans remains relatively uncertain. Indeed, adipose tissue insulin resistance is a particularly exciting topic of active exploration (176). WAT is adapted to store excess energy and can do so prolifically without inducing metabolic derangements [evidenced most dramatically by the adiponectin transgenic ob/ob mouse, which remains normally insulin sensitive despite morbid obesity (408)]. As a result, some paradigms of nutrient stress well characterized in skeletal muscle and liver, such as lipidinduced insulin resistance, do not obviously translate to the white adipocyte. Gross measurement of tissue lipids such as White adipose tissue Liver INSR Hepatic glucose production Muscle insulin resistance DAG/PKCθ signaling Gluconeogenesis DAG/PKCε signaling INSR Acetyl CoA β-oxidation β-oxidation PC Glycogen synthesis IMCL Hepatic insulin resistance Glycogen synthesis Glucose transport Skeletal muscle Plasma glucose IHTG NEFA NEFA Glycerol Macrophage infiltration Nutrient stress Adipocyte death TNFα IL-1β ? NEFA Overnutrition Adipose insulin resistance INSR RBP4 JNK Glycerol TAG NEFA Lipolysis Glycerol Acetyl CoA β-oxidation FIGURE 19. An integrated physiological perspective on tissue insulin resistance. Chronic overnutrition is the ultimate cause of systemic insulin resistance and promotes insulin resistance by both tissue-autonomous and crosstalk-dependent mechanisms. Chronic overnutrition promotes lipid accumulation in skeletal muscle and liver, which causes insulin resistance in those tissues. Additionally, chronic overnutrition poses a nutrient stress to adipocytes, resulting in adipocyte insulin resistance and adipocyte death. Increases in the adipokine RBP4 and other proinflammatory signals lead to the recruitment of macrophages to white adipose tissue. Inflammatory signaling in macrophages, including activation of c-Jun NH2-terminal kinase (JNK), leads to the elaboration of paracrine mediators such as tumor necrosis factor- (TNF), interleukin-1 (IL-1), and others. These inflammatory cytokines may increase adipocyte lipolysis either directly or indirectly by impairing insulin signaling. The increased adipocyte lipolysis of inflammation increases nonesterified fatty acid (NEFA) and glycerol turnover. This has direct (glycerol conversion to glucose) and indirect [NEFA-derived acetyl CoA activation of pyruvate carboxylase (PC)] stimulatory effects on gluconeogenesis, and also promotes accumulation of intrahepatic triglyceride (IHTG) and consequent lipid-induced hepatic insulin resistance, which impairs insulin stimulation of net hepatic glycogen synthesis. Together, these effects increase hepatic glucose production. Chronically increased lipolysis may also facilitate the accumulation of intramyocellular lipid (IMCL) and consequent lipid-induced muscle insulin resistance. The decreased glucose disposal of muscle insulin resistance increases glucose availability for the liver, which in turn promotes IHTG accumulation and worsens

Arabic

في حين أن الكربوهيدرات، التي توفر الجلوكوز للجسم لدعم عملية التمثيل الغذائي، هي حاسمة للنظام الغذائي، تناول غير مناسب يمكن أن يؤدي إلى ارتفاع السكر في الدم، ونقص السكر في الدم، وتقلبات نسبة السكر في الدم التي تضر النتائج الصحية (الشكل 2). الشكل 2- الأرباح التي يمكن أن تتراوح بين 2 و 2 عواقب عدم توازن الجلوكوز. A. فرط السكر في الدم (ارتفاع مستوى السكر في الدم) قد تسهم في تعزيز الدهون والعضلات الأيض; بالإضافة إلى ذلك ، يفضل فرط السكر في الدم مضاعفات في حالات الأمراض الحادة بما في ذلك الجراحة والأمراض الخطيرة.

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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

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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

Arabic

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

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Plasma Metabolic Variables. Plasma insulin concentration was almost 2-fold greater and plasma adiponectin concentration was ≈50% lower in subjects with high IHTG content than in those with normal IHTG who were matched on VAT volume (Table 2). No significant differences in metabolic variables were detected between subjects with low or high VAT volume who were matched on IHTG content (Table 2). Table 2. Table 2. 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 informatio

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Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity Elisa Fabbrini, Faidon Magkos, [...], and Samuel Klein Additional article information Associated Data Supplementary Materials ABSTRACT Visceral adipose tissue (VAT) is an important risk factor for obesity-related metabolic disorders. Therefore, a reduction in VAT has become a key goal in obesity management. However, VAT is correlated with intrahepatic triglyceride (IHTG) content, so it is possible that IHTG, not VAT, is a better marker of metabolic disease. We determined the independent association of IHTG and VAT to metabolic function, by evaluating groups of obese subjects, who differed in IHTG content (high or normal) but matched on VAT volume or differed in VAT volume (high or low) but matched on IHTG content. Stable isotope tracer techniques and the euglycemic–hyperinsulinemic clamp procedure were used to assess insulin sensitivity and very-low-density lipoprotein–triglyceride (VLDL-TG) secretion rate. Tissue biopsies were obtained to evaluate cellular factors involved in ectopic triglyceride accumulation. Hepatic, adipose tissue and muscle insulin sensitivity were 41, 13, and 36% lower (P < 0.01), whereas VLDL-triglyceride secretion rate was almost double (P < 0.001), in subjects with higher than normal IHTG content, matched on VAT. No differences in insulin sensitivity or VLDL-TG secretion were observed between subjects with different VAT volumes, matched on IHTG content. Adipose tissue CD36 expression was lower (P < 0.05), whereas skeletal muscle CD36 expression was higher (P < 0.05), in subjects with higher than normal IHTG. These data demonstrate that IHTG, not VAT, is a better marker of the metabolic derangements associated with obesity. Furthermore, alterations in tissue fatty acid transport could be involved in the pathogenesis of ectopic triglyceride accumulation by redirecting plasma fatty acid uptake from adipose tissue toward other tissues. Keywords: abdominal fat, insulin resistance, NAFLD, steatosis, VLDL Visceral adipose tissue (VAT) is an important and independent predictor of metabolic risk factors for coronary heart disease, particularly diabetes and dyslipidemia (1, 2). Moreover, data from metabolic studies conducted on human subjects (3, 4) indicate that an increase in VAT is associated with impaired glucose tolerance, insulin resistance, and increased very-low-density lipoprotein–triglyceride (VLDL-TG) secretion. These observations and the unique anatomical location of visceral fat, which releases free fatty acids (FFA) and adipokines into the portal vein for direct transport to the liver, have led to the concept that VAT is responsible for many of the metabolic abnormalities associated with abdominal obesity (5, 6). Therefore, a reduction in visceral fat has become a key therapeutic goal in the management of obesity (6, 7). Although VAT is associated with metabolic disease, a causal link between VAT and metabolic dysfunction has not been demonstrated in humans. Recently, it has become clear that VAT correlates directly with intrahepatic triglyceride (IHTG) content (8–10), and an increase in IHTG is associated with the same metabolic abnormalities linked to an increase in VAT (9–12). Therefore, it is possible that VAT itself is not harmful, but is simply an innocent bystander that tracks with IHTG. The mechanism(s) responsible for the interrelationship among IHTG content, insulin resistance, and hypertriglyceridemia is not known, but could involve redirecting plasma FFA uptake and intracellular triglyceride production from adipose tissue depots to other tissues, such as liver and skeletal muscle, which can impair insulin signaling (13, 14) and stimulate VLDL-TG secretion (11). Therefore, it is possible that organ-specific alterations in CD36, which regulates tissue FFA uptake from plasma (15), are involved in the pathogenesis of ectopic triglyceride accumulation and metabolic disease. The purpose of the present study was to test the hypotheses that (i) high IHTG content, not increased VAT volume, is the primary marker of metabolic abnormalities associated with obesity and (ii) high IHTG content is associated with alterations in adipose tissue and skeletal muscle CD36 gene expression and protein content that are consistent with redirecting plasma fatty acids away from adipose tissue and toward other metabolic organs. Both in vivo and cellular metabolic assessments were conducted in obese subjects, who were carefully matched on either IHTG content or VAT volume, to help separate the potential influence of IHTG and VAT on metabolic function. Stable isotope tracer infusions in conjunction with mathematical modeling were used to evaluate hepatic, skeletal muscle and adipose tissue insulin sensitivity, and VLDL-TG secretion rate, while adipose tissue and skeletal muscle biopsies were used to determine cellular CD36 gene expression and protein content. RESULTS Body Composition. Subjects in each group were matched on age, sex, body mass index (BMI), and percentage of body fat, but differed in either IHTG content or VAT volume (Table 1). Mean IHTG content in the high-IHTG groups was 5-fold greater than in the normal-IHTG groups, and mean VAT volume in the high-VAT group was 2-fold greater than in the low-VAT group (Table 1). Table 1. Table 1. Subject characteristics in each study group Plasma Metabolic Variables. Plasma insulin concentration was almost 2-fold greater and plasma adiponectin concentration was ≈50% lower in subjects with high IHTG content than in those with normal IHTG who were matched on VAT volume (Table 2). No significant differences in metabolic variables were detected between subjects with low or high VAT volume who were matched on IHTG content (Table 2).

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==See also==*Progressive familial intrahepatic cholestasis==References====External links==* Official Website for the Alagille Syndrome Alliance* Official Alagille Syndrome Alliance message board* GeneReviews/NCBI/UW/NIH entry on Alagille syndrome* OMIM entries on Alagille syndrome*Alagille Syndrome, Liver Diseases and Treatments, Cincinnati Children's Hospital Medical Center*Information from the Alagille Syndrome Alliance* Children's Liver Disease Foundation"This article incorporates public domain text from The U.S. National Library of Medicine"

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2-"الجراحة":== المصادر ==http://www.emedicine.com/ped/TOPIC60.HTMhttp://www.ikp.unibe.ch/lab2/Alagille.htm* Official Website for the Alagille Syndrome Alliance* Official Alagille Syndrome Alliance message board* GeneReviews/NCBI/UW/NIH entry on Alagille syndrome* OMIM entries on Alagille syndrome* Alagille Syndrome, Liver Diseases and Treatments, Cincinnati Children's Hospital Medical Center* Information from the Alagille Syndrome Alliance* Children's Liver Disease Foundation

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