Metabolic and Nutritional Profile of Obese Adolescents With Nonalcoholic Fatty Liver Disease

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Metabolic and Nutritional Profile of Obese Adolescents WithNonalcoholic Fatty Liver Disease

Aline de Piano, Wagner L. Prado, Danielle A. Caranti, Kali O. Siqueira, Sergio G. Stella,Mara Lofrano, Lian Tock, Dejaldo M.J. Cristofalo, Henrique Lederman, Sergio Tufik,

Journal of Pediatric Gastroenterology and Nutrition44:446–452 # 2007 by European Society for Pediatric Gastroenterology, Hepatology, and Nutrition andNorth American Society for Pediatric Gastroenterology, Hepatology, and Nutrition

right © 2007 by

Marco Tulio de Mello, and Ana R. Damaso

3-day inquiry.

arterial hypertensionand cardiovascularmainly in the form of

Received May 15, 200Address corresponden

Damaso, Rua Marselhes04020-060, Brazil (e-mai

Financial support was r2006/00684-3, CENESP,S.T), UNIFESP, and the CProgram.

l University of Sao Paulo, Escola Paulista de Medicina UNIFESP-EPM, Sao Paulo, B
Federa razil
ABSTRACT

Background: The incidence of nonalcoholic fatty liver disease(NAFLD) is increasing due to its prevalence in obesity,diabetes, and insulin-resistance syndrome. The besttreatment protocol for NAFLD has not been determined.However, there is evidence that exercise and nutritionalintervention can improve and prevent it. The aim of thepresent study was to evaluate the dietary and metabolicprofiles of obese adolescents with NAFLD who participatedin a multidisciplinary program.Patients and Methods: We studied 43 adolescents ages 15 to19 years (17.18� 1.66 years) with a body mass index (BMI)�30, consisting of 30 patients without NAFLD (BMI¼35.80� 3.44 kg/m2) and 13 with NAFLD (BMI¼ 33.47�2.34 kg/m2). The NAFLD diagnosis was determined byultrasonography. Blood samples were collected to analyzeglycemia, hepatic aminotransferase levels, and lipid profiles.Insulin resistance was measured by homeostasis model

Lippincott Williams & Wilkins.Un

, type 2 diabetes mellitus, cancer,mortality (4–8). Body fat excess,central obesity, is closely correlated

6; accepted January 17, 2007.ce and reprint requests to Nadja Ana R.a no. 535-Vila Clementino, Sao Paulo/SPl: [email protected]).eceived from AFIP, CNPq, CAPES, FAPESPFADA, FAPESP (CEPID/Sleep #9814303-3EPE Multidisciplinary Obesity Intervention

446

Results: At baseline conditions, the patients with NAFLDshowed significant differences in body mass, BMI, and vis-ceral and subcutaneous fat. Glucose and visceral and subcutane-ous fat presented a significant reduction after treatment inpatients with NAFLD. Analyzing the food intake, at baselinewe observed a positive correlation between the visceral obesityand lipid consumption only in patients with NAFLD. We alsoobserved significant decrease in energy and cholesterol con-sumption in patients with NAFLD after the multidisciplinarytherapy.Conclusions: The intervention promoted a decrease in theprevalence of NAFLD, a significant decrease in visceralobesity, and improved HOMA-IR, glycemia, and serum lipidlevels that are risk factors for NAFLD. In summary, themultidisciplinary program is essential in the treatment andprevention of NAFLD. JPGN 44:446–452, 2007. Key Words:Food intake—Nutrition—Visceral adipose tissue. # 2007 by

assessment insulin-resistance index (HOMA-IR). The analyses
European Society for Pediatric Gastroen of baseline and postintervention food intake were made by a
terology, Hepatology,and Nutrition and North American Society for Pediatric
Gastroenterology, Hepatology, and Nutrition
INTRODUCTION

Obesity is increasing worldwide, especially in adoles-cents, affecting more than 15% of Brazilian children andadolescents (1–3). Studies have shown the relationshipbetween obesity and several diseases in adult life, such as

with dyslipidemia, high blood pressure, hyperinsuline-mia, and high fasting glucose levels (7,9,10).

The visceral obesity increases plasma free fatty acid(FFA) levels because these adipocytes have higher lipo-lytic activity. Consequently, the visceral obesity increasesthe FFA levels in the portal circulation, and insulinresistance can also be responsible for this increase(7,11). A large amount of FFA increases triglyceridesserum levels, and may exceed the very low–densitylipoprotein (VLDL) synthetic capacity, promotingstorage in the liver, known as fatty liver (12).

Nonalcoholic fatty liver disease (NAFLD) is an emer-ging clinical problem among patients of all ages. NAFLDincludes a broad spectrum of liver tissue alterations,

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ranging from pure steatosis to cirrhosis (13,14) tononalcoholic steatohepatitis (NASH). NASH is definedby the presence of lobular necroinflammatory activity

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with or without the presence or perisinusoidal fibrosisthat can evolve to cirrhosis and can be detected on liverbiopsy (15). Differentiating between the 2 is importantbecause as many as 28% of patients with steatohepatitis,in contrast to those with simple steatosis, may progress tocirrhosis, but the only reliable method of differentiatingthem is by biopsy, which is costly and carries risks topatients (16). Therefore, ultrasonography (US), a non-invasive method to diagnose NAFLD in an ambulatorycare setting, is common (17–21).

Considering the grading for steatosis, a variation fromgrades I to III was observed (grade I, <33%; grade II,33%–66%, and grade III, >66% of hepatocytes areaffected) (20). NAFLD affects 10% to 39% of the worldpopulation, 50% of diabetic patients, 57% to 74% ofobese people, and as many as 90% of morbidly obesepeople (13,14). The prevalence in obese adolescents isbetween 22.5% and 52.8% (20,22–24).

The treatment of NAFLD is based on the associatedfactors of the disease and consists of gradual body massreduction, glycemia, and lipid control (ie, cholesteroland triglycerides). The main goal is not only to treat thefatty liver disease but also obesity, diabetes, and hyper-lipidemia (25–28). Although there is no accepted treat-ment that can reverse fatty liver disease, all patientsshould be given a low-fat diet and triglyceride-loweringagents. They should also be encouraged to exerciseregularly (6).

Because of the scarcity of studies related to theinfluence of diet on NAFLD, the purpose of this studywas to assess the short-term (12 weeks) effect of amultidisciplinary program on the dietary and metabolicprofiles of obese adolescents with NAFLD.

PATIENTS AND METHODS

Population

A total of 43 postpuberes obese adolescents (19 boys and24 girls) were recruited. Their ages ranged from 15 to 19 years,and their BMI was 34.22� 2.93 kg/m2. The inclusion criteriawere pubertal stage as assessed by means described by Tanneret al (29) and severe primary obesity (body mass index [BMI]>30), and agreement by the adolescents and their families toparticipate in a 12-week multidisciplinary weight loss program.The exclusion criteria were identified as genetic, metabolic, orendocrine disease; chronic alcohol consumption; previous druguse; and other causes of liver steatosis. The subjects volunteeredin response to statements on radio and television and in localnewspapers.

This study was carried out in accordance with the principlesof the Declaration of Helsinki and was formally approved by theethical committee of the Federal University of Sao Paulo

METABOLIC AND NUTRITIONAL PROFILE

yright © 2007 by Lippincott Williams & Wilkins.U

Paulista Medicine School (#0135/04). Informed consent wasobtained from all subjects and/or their parents. All subjectsunderwent electrocardiography.

Study Protocol

During the first visit, subjects were medically screened, hadtheir pubertal stage assessed, and had their anthropometricsprofile measured (height, weight, BMI, and body composition).During the second visit a blood sample was collected andanalyzed for various variables. At the third visit US wasperformed. The patients were divided into 2 groups: NAFLD(n¼ 13) and non-NAFLD (n¼ 30). For each subject, theprocedures were scheduled for the same time of day and atleast 15 hours after the last training session to remove anyinfluence of diurnal variations. Thereafter, obese adolescentsstarted the multidisciplinary weight loss program, as describedin the subsequent sections.

Anthropometric Measurements and BodyComposition

Subjects were weighed wearing light clothing and no shoeson a Filizola scale to the nearest 0.1 kg. Height was measured tothe nearest 0.5 cm by using a wall-mounted stadiometer(Sanny, model ES 2030). BMI was calculated as body weightdivided by height squared. Body composition was estimated byplethysmography in the BOD POD body composition system(version 1.69; Life Measurement Instruments, Concord, CA)(30).

Serum Analysis

Blood samples were collected in the outpatient clinic atapproximately 8:00 AM after an overnight fast. Insulinresistance was assessed by homeostasis model assessmentinsulin-resistance index (HOMA-IR). HOMA-IR was calcu-lated by the fasting blood glucose (FBG) and the immuno-reactive insulin (I): [FBG (mg/dL) � I (mU/L)]/405. Totalcholesterol, high-density lipoprotein (HDL), triacylglycerol,and hepatic alanine aminotransferase were analyzed using acommercial kit (CELM, Barueri, Brazil). The HOMA-IR, lipidserum level, and aminotransferase data were analyzed accord-ing to reference values described by Schwimmer et al (31).

Hepatic Steatosis and Visceral and SubcutaneousAdiposity Measurements

All abdominal US procedures and measurements of visceraland subcutaneous fat tissue and fatty liver before and afterintervention were performed in a double-blinded fashion by thesame physician specializing in image diagnostic using a3.5-MHz multifrequency transducer (broadband). This pro-cedure permits a reduction of risk margin for misclassification.The intraexamination coefficient of variation for US was 0.8%.

The US measurements of intraabdominal (ie, visceral) andsubcutaneous fat were taken. US-determined subcutaneous fatwas defined as the distance between the skin and external faceof the rectus abdominis muscle, and visceral fat was defined asthe distance between the internal face of the same muscle and

OBESE ADOLESCENTS WITH NAFLD 447

nauthorized reproduction of this article is prohibited.

the anterior wall of the aorta. Cutoff points to define visceralobesity by US parameters were based on previous methodo-logical descriptions by Ribeiro-Filho et al (32).

J Pediatr Gastroenterol Nutr, Vol. 44, No. 4, April 2007

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34 subjects (24 without NAFLD and 10 with NAFLD)because 9 patients dropped out of the program. Indeed,the dietary data were available for only 23 subjects

30,23

69,77

18,6

81,4

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20

40

60

80

100

AfterBaseline

With NAFLDWithout NAFLD

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The US definition of fatty liver was based on previouslyreported diagnostic criteria and detected liver steatosis wasclassified as grade I (liver attenuation slightly less than spleen),grade II (more pronounced difference between liver and spleenand intrahepatic vessels not seen or slightly higher attenuationthan liver), or grade III (markedly reduced liver attenuation withsharp contrast between liver and intrahepatic vessels) (19,22).In the present study the group with NAFLD presented withsome liver steatosis diagnosed by US, and all of the patientspresented with normal alanine aminotransferase levels, whichwas diagnosed as simple steatosis.

Medical Program

To accomplish their health and clinical parameters, thepatients visited the endocrinologist once per month.

Dietary Program

Energy intake was set at the levels recommended by thedietary reference intake for subjects with low levels of physicalactivity of the same age and sex (33). However, no fixed level ofenergy intake was prescribed; they were encouraged only toreduce their food intake and follow a balanced diet. No drugsand antioxidants were recommended.

Once each week, adolescents attended dietetics classes thatincluded information on the food pyramid, recording energyunits intake, weight loss, dieting, diet versus ‘‘light,’’ fat andcholesterol, and nutrition facts.

At the beginning and end of the 12-week program, a 3-daydietary record was made by all of the adolescents with the helpof their parents because most obese people underreport theirfood consumption (34). The degree of underreporting may besubstantial; however, this is a valid method of evaluatingnutrition consumption (35). Portions were measured in termsof familiar volume and size and by reference to an atlas of localfood portions. The dietitian taught the parents and adolescentshow to record food consumption. These dietary data weretransferred to a computer by the same dietitian, and nutrientcomposition was analyzed by a software program developed atthe Federal University of Sao Paulo Paulista Medicine School(Nutwin software for Windows, version 1.5, 2002) basedon Western and local food tables. In addition, the parentswere encouraged by a dietitian to call if they needed extrainformation.

Exercise Program

During the 12-week multidisciplinary intervention period,adolescents followed a personalized aerobic training programincluding 60-minute sessions 3 times per week (180 minutes/week) under the supervision of a sports therapist. Each programwas developed according to the results of an initial oxygenuptake test for aerobic exercises (cycle ergometer andtreadmill). The intensity was set at a workload correspondingto ventilatory threshold 1 (50%–70% of oxygen uptake test). Atthe end of 6 weeks, aerobic tests were performed to assessphysical capacities and to adjust physical training intensity

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right © 2007 by Lippincott Williams & Wilkins.Un

individually (data not shown). During the aerobic sessions,adolescents underwent heart rate monitoring. The exerciseprogram was based on the American College of Sports


Medicine position statement of 2001 (36). Information aboutlifestyle changes related to activity was also provided andspontaneous physical activity (eg, walking, stair climbing)was encouraged but not measured.

Psychological Intervention

A diagnosis was established by validated questionnairesconsidering some psychological problems caused by obesitythat have been described in the literature, such as depression,disturbances of body image, anxiety, and decrease ofself-esteem. During the multidisciplinary intervention, theadolescents attended weekly psychological orientation groupsessions in which they discussed body image and alimentarydisorders such as bulimia and anorexia nervosa; binge eating;their signals, symptoms, and consequences for health; relationbetween feelings and food; familiar problems such asalcoholism; and other topics. An individual psychologicaltherapy was recommended when we found nutritional andbehavioral problems.

Statistical Analysis

All data were analyzed by means of Statistica version 6 forWindows with significance set at P< 0.05. All of the data areexpressed as mean� SD unless otherwise stated.

Comparisons between measures at baseline and after theweight loss program were made using paired t tests, betweengroups by independent t tests, and Pearson correlation.

RESULTS

The present study comprised 43 obese adolescentsdivided into 30 patients without NAFLD and 13 withNAFLD. The prevalence of NAFLD was 30.23% in thispopulation, but only 18.6% at the end of the multidisci-plinary program (Fig. 1).

Complete data after the intervention were available for

ET AL.


intervention

FIG. 1. Prevalence of NAFLD (%) in obese adolescents at base-line and after multidisciplinary weight loss program.

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TABLE 1. Anthropometric, subcutaneous, and visceral adipose tissues; HOMA-IR; lipids; and waist circumference data in obeseadolescents with and without NAFLD before and after intervention for weight loss

Variable

Patients without NAFLD

P

Patients with NAFLD

PBaseline (n¼ 30) After intervention (n¼ 24) Baseline (n¼ 13) After intervention (n¼ 10)

Body mass, kg 92.32� 11.60 89.41� 10.93 0.002 102.76� 8.48�

95.73� 6.30 NSBMI, kg/m2 33.47� 2.34 32.46� 2.64 0.01 35.80� 3.44

�33.89� 4.64 NS

Visceral fat, cm 3.44� 1.22 3.16� 1.13 NS 4.29� 0.75�

3.09� 1.15 0.02Subcutaneous fat, cm 2.93� 0.59 2.73� 0.60 0.0002 3.4� 0.59

�2.91� 0.95 0.005

Glucose, mg/dL 92.17� 5.49 88.26� 6.18 0.02 94.1� 7.07 89.6� 6.61 0.009Insulin, mU/dL 14.95� 7.18 12.15� 5.59 NS 18.85� 6.87 16.6� 8.3 NSHOMA-IR 3.29� 1.63 2.62� 0.11 0.03 4.18� 1.52 3.69� 2.29 NSTotal cholesterol, mg/dL 165.73� 32.46 154.59� 64.34 0.003 175.3� 31.80 150.90� 19.87 NSTriglycerides, mg/dL 125.4� 58.54 101.40� 52.65 0.03 109.46� 57.49 115.6� 59.09 NSHDL, mg/dL 49.86� 10.76 49.09� 8.96 NS 45.15� 7.41 45.7� 6.94 NSLDL, mg/dL 90.80� 25.10 85.22� 27.66 NS 108.38� 32.54 82.10� 20.95 NSWaist, cm 94.96� 7.4 93.57� 7.19 NS 98.95� 7.58 96.73� 7.87 NS

P� 0.(<2.0)

METABOLIC AND NUTRITIONAL PROFILE OF OBESE ADOLESCENTS WITH NAFLD 449

(18 without NAFLD and 5 with NAFLD) because 11 ofthem did not fill out the 3-day inquiry.

Anthropometrics, Body Fat, Glucose, Insulin,HOMA-IR, Lipid Serum Levels, and Waist

Comparing the 2 groups at baseline conditions, thepatients with NAFLD had higher values in allcategories. However, only body mass, BMI, and visceraland subcutaneous fat showed significant differences.Glucose and visceral and subcutaneous fat presented asignificant reduction after treatment in patients withNAFLD. In the same way, body mass, BMI, glucose,subcutaneous fat, HOMA-IR, cholesterol, and triglycer-ides decreased significantly in patients without NAFLD(Table 1).

Food Intake

At baseline conditions, no significant differences in allnutrient values were observed between the groups with

�Group with NAFLD vs group without NAFLD for the same time,

Reference values: glucose (60–110 mg/dL), insulin (<20), HOMA-IR(>38 mg/dL), and LDL (<130 mg/dL) (31).


and without NAFLD. However, carbohydrate, protein,and cholesterol consumption were higher in patients withNAFLD. We observed a significant decrease in energy

TABLE 2. Characteristics of food intake measured at baseline and awith and withou

Nutrients

Patients without NAFLD (n¼ 30)

Baseline (n¼ 30) After intervention (n¼ 18)

Energy intake, kcal 1866.6� 633.75 1574.29� 556.08Carbohydrate, % 51.84� 8.16 52.35� 7.09Protein, % 22.24� 7.51 22.99� 6.64Lipid, % 25.91� 7.71 24.72� 6.48Cholesterol, mg 245.12� 136.95 227.22� 74.45

and cholesterol consumption in patients with NAFLDafter the multidisciplinary therapy (Table 2).

No significant difference was observed in lipidconsumption between the 2 groups at baseline conditions,but we did observe a positive correlation only betweenvisceral obesity and lipid consumption of patients withNAFLD (Fig. 2).

DISCUSSION

Obesity is strictly related to the development ofNAFLD. Several recent reviews showed that thereduction of weight and changes in lifestyle couldpromote an improvement in fatty liver, and data fromthe present study corroborated the results of these studies.We also analyzed a possible relationship between dietarycomposition and the development of this disease. Hence,the multidisciplinary program to treat obese adolescentsis highly important (25–27). These studies did not show acorrelation between visceral obesity and lipid ingestion,however.

05., total cholesterol (<170 mg/dL), triglycerides (33–129 mg/dL), HDL


In the present study 30.23% of obese adolescents had adiagnosis NAFLD, which is similar to values observed byother authors. After the 12-week intervention, there was a

fter multidisciplinary weight loss program in obese adolescentst NAFLD

P

Patients with NAFLD (n¼ 13)

PBaseline (n¼ 13) After intervention (n¼ 5)

NS 1620.74� 399.12 1328.38� 422.44 0.010NS 52.69� 6.89 55.06� 3.77 NSNS 23.75� 3.74 24.19� 3.59 NSNS 23.55� 8.46 20.67� 3.47 NSNS 253.54� 86.07 195.12� 94.13 0.018


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r = 0.61

36343230282624222018161412lipid consumption (%)

2,8

3,0

3,2

3,4

3,6

3,8

4,0

4,2

4,4

4,6

4,8

5,0

5,2

5,4

5,6

5,8

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18.6% reduction in the prevalence of NAFLD (Fig. 1). Alimitation of the present study was the lack of histologicaldata, which would better describe the actual effect of theintervention on the prevalence and grade of NAFLD.However, there is increasing interest in US-diagnosedNAFLD in the ambulatory care setting (17–21).

NAFLD is strongly associated with features ofmetabolic syndrome, including insulin resistance,impaired glucose tolerance, and dyslipidemia (37–42).It has also been proposed that visceral obesity may be amajor contributor to fatty liver in the insulin-resistantstate. As such, evaluation of these metabolic parametersis essential in obese adolescents. When we compared the2 groups at baseline conditions, we observed a significantdifference in body fat composition. The patients withNAFLD showed higher values for body mass, BMI, andvisceral and subcutaneous fat; however, our study waseffective in promoting a significant reduction in visceraland subcutaneous fat in patients with NAFLD. Thereduction in visceral obesity in patients with NAFLDis important because several studies suggest that theadipose tissue may be a major source of massive freefatty acid flow to the liver. Indeed, visceral obesity ismore influential than body mass in predicting fatty liver(20,39,43). Subjects with more pronounced visceralobesity appear to be at greater risk for fatty liver becauseof their ability to transport free fatty acids directly intothe portal vein for conversion to triglycerides within theliver (19,44–46).

Insulin resistance causes alterations in the uptake,degradation, and/or secretion of lipid molecules, whichleads to the accumulation of lipids in the hepatocytes.Studies have observed that patients with NAFLD had

FIG. 2. Correlation between visceral fat and lipid consumption inobese adolescents with NAFLD at baseline conditions.


insulin resistance (14,28,46–48). Glycemia presented asignificant reduction in both groups after the interven-tion, but the values were normal at the beginning of the


present study. We observed altered values of insulin in38.46% in the group with NAFLD and 26.6% in the groupwithout NAFLD. Analyzing the insulin resistance byHOMA-IR, we noticed a higher prevalence in theNAFLD group (92.3%) compared with the group withoutNAFLD (76.7%). It is also generally believed thatNAFLD is a metabolic disorder and that insulin resist-ance plays a key role in its genesis. Insulin resistance,along with other potential biochemical abnormalities,results in fatty liver and the generation of excessive freeradicals in the liver, which produce liver injury (49).

Cholesterol and triglycerides showed a significantdecrease after the intervention in patients withoutNAFLD. Indeed, we observed decreases in total choles-terol (13.9%), LDL (9.58%), HOMA-IR (11.7%), andwaist circumference (2.24%), as well as increased HDL(1.2%) in patients with NAFLD. Conversely, atthe beginning of treatment, the serum lipid levelmeasurements presented normal values in both groupsexcept the total cholesterol of patients with NAFLD.

There is evidence that the diet composition caninfluence the development and improvement of NAFLD.Studies suggest that a hypocaloric diet that promotes areduction of 5% to 10% of body mass decreases lipidintake, and increased antioxidants can contribute to thetreatment of NAFLD (37,50–54).

In Table 1, patients with NAFLD were heavier at base-line (102.76 kg) than patients without NAFLD (92.32 kg).Conversely, the group with NAFLD consumed fewerenergy units (1620.74 kcal/d) than the group withoutNAFLD (1866.6 kcal/d). A possible explanation is thatelevated levels of leptin are found in the majority ofpatients with NAFLD (55). It may contribute to leptinresistance and low ghrelin concentrations, suggesting adecrease in energy expenditure and food intake. In fact,previous research by our group reinforces this hypothesis(56).

Although no significant differences in food intakewere observed between the 2 groups, in patients withNAFLD there was a reduction in lipid consumption from23.55% to 20.67% and a significant reduction in totalenergy intake (from 1620.74 kcal� 399.12 to 1328.38kcal� 422.44) and cholesterol (from 253.54� 86.07 to195.12� 94.13). This result can be partially explainedbecause the adolescents decreased portion sizes mainlyin foods that are sources of lipids. Consequently, thenutritional intervention contributed to improve lipidingestion in patients with NAFLD, which plays animportant role in the development of this disease.However, other investigations pointed out that thesubjectivity of food-recording techniques may be asource of error. A number of investigators think thatunderrecording of self-reported food intake often occurs,

ET AL.


and that participation in a weight management studyleads to subconscious underestimation and/or underre-porting of total daily energy intake (57).

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One of the most important findings of our study is thatdespite the lipid consumption at baseline conditions,there was no significant difference between the patientswith and without NAFLD, and a positive correlation(0.61) between lipid consumption and visceral obesitywas observed only in patients with NAFLD (Fig. 2).Although the r value was not extremely strong, itrepresents an important positive correlation that hasnot been discussed in the literature to our knowledgeand requires further investigation with better patientsamples.

The key observation in this clinical study is that thepatients with NAFLD accumulated more visceral fatand presented more altered insulinemia and higherHOMA-IR values than patients without NAFLD(Table 1). Under these conditions there is a disproportio-nately greater flow of free fatty acids from visceraladipose stores, which are transported to the liver byportal blood and affect hepatic lipid and glucose metab-olism and insulin sensitivity, causing insulin resistance(9,10,25,58,59). These mechanisms contribute to thedevelopment of NAFLD. It provides a unifying mech-anism that links the coordinated regulation of glucose andlipid metabolism in the liver by hormonal regulation oflipolysis in visceral adipose stores (49). This way,reduction in the HOMA-IR, visceral obesity, and lipidingestion is essential to prevent and treat fatty liverdisease.

CONCLUSIONS

The multidisciplinary intervention promoted a decreasein the prevalence of NAFLD, a significant decrease in thevisceral obesity, and improved HOMA-IR, glycemia, andlipid serum levels that are risk factors for NAFLD. Thepatients with NAFLD presented higher anthropometrics,visceral and subcutaneous fat, HOMA-IR, total choles-terol, LDL and waist values at baseline conditions. Afterthe intervention all of the values, except HOMA-IR,were normalized in both groups. No significant differenceswere observed in the food intake between the 2 groups,however the lipid consumption of patients with NAFLDwas correlated with visceral obesity. In summary, themultidisciplinary program, including the nutritionalintervention, is essential in the treatment and preventionof NAFLD.

Acknowledgment: The authors thank the patients and theirparents for their participation in this study.

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Metabolic and Nutritional Profile of Obese Adolescents With Nonalcoholic Fatty Liver Disease

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