Current treatment strategies for obesity: pharmacological and non-pharmacological approaches

Obesity is a multifactorial and complex condition that is characterized by abnormal and excessive white adipose tissue accumulation, which can lead to the development of metabolic diseases, such as type 2 diabetes mellitus, nonalcoholic fatty liver disease, cardiovascular diseases, and several types of cancer. Obesity is characterized by excessive adipose tissue accumulation and associated with alterations in immunity, displaying a chronic low-grade inflammation profile. Adipose tissue is a dynamic and complex endocrine organ composed not only by adipocytes, but several immunological cells, which can secrete hormones, cytokines and many other factors capable of regulating metabolic homeostasis and several critical biological pathways. Remarkably, adipose tissue is a major source of circulating microRNAs (miRNAs), recently described as a novel form of adipokines. Several adipose tissue–derived miRNAs are deeply associated with adipocytes differentiation and have been identified with an essential role in obesity-associated inflammation, insulin resistance, and tumor microenvironment. During obesity, adipose tissue can completely change the profile of the secreted miRNAs, influencing circulating miRNAs and impacting the development of different pathological conditions, such as obesity, metabolic syndrome, and cancer. In this review, we discuss how miRNAs can act as epigenetic regulators affecting adipogenesis, adipocyte differentiation, lipid metabolism, browning of the white adipose tissue, glucose homeostasis, and insulin resistance, impacting deeply obesity and metabolic diseases. Moreover, we characterize how miRNAs can often act as oncogenic and tumor suppressor molecules, significantly modulating cancer establishment and progression. Furthermore, we highlight in this manuscript how adipose tissue–derived miRNAs can function as important new therapeutic targets.

Waist Circumference and Insulin Resistance Are the Most Predictive Metabolic Factors for Steatosis and Fibrosis

Introduction: About 30% of all U.S. adults and 70-80% of those with Type 2 diabetes mellitus (T2DM) have non-alcoholic fatty liver disease (NAFLD). Atherosclerotic cardiovascular disease (CVD) is more common among NAFLD patients, albeit with limited evidence from large prospective studies. Hypothesis: American Indians (AI) with NAFLD would be more likely to develop carotid atherosclerosis given their high prevalence of obesity and T2DM. Methods: The Strong Heart Family Study (SHFS) is a population-based family study of CVD and its risk factors in AI. Participants (n=2786; 59.6% female, mean age 40.8 ±17.3 y) were recruited from 12 tribes in 3 regions: Arizona, North/South Dakota, and Oklahoma. Carotid ultrasound-assessed plaque and plaque score were obtained at the baseline examination in 2001-03, and again in surviving participants (n=2406) from 2006 to 2009. NAFLD prevalence was estimated using hepatic steatosis index (HSI). NAFLD fibrosis score was used to separate NAFLD patients with or without advanced fibrosis. HSI is calculated using serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), BMI, diabetes status, and sex, while the NAFLD fibrosis score is derived from age, BMI, diabetes status, ALT, AST, platelet count, and serum albumin. Plaque progression was defined as any increase in plaque score (0 to 8 carotid segments with plaque) from baseline to the second examination. Frailty model was used in data analyses to account for the relatedness among family members. Results: Mean BMI of participants was 31.3 ± 7.5 kg/m 2 , 19% had T2DM, 32.6% were hypertensive, and 36.3% were current smokers. NAFLD prevalence (HSI > 36) was 78%, while 6% did not have NAFLD (HSI < 30) and 16% participants were in an intermediate category (HSI 30-36). Among participants with NAFLD (n=2096), three fibrosis classes were defined by NAFLD fibrosis scores: 1 no to moderate fibrosis (61%, fibrosis score < -1.455), 2 indeterminate (31%, -1.455 ≤ fibrosis score ≤ 0.676), and 3 cirrhosis or severe cirrhosis (8%, fibrosis score > 0.676). About 31% of participants had carotid atherosclerosis (plaque score ≥ 1) at baseline. About 14% of the 2252 participants who had two carotid ultrasound evaluations had plaque progression and 19% of those without carotid atherosclerosis at baseline (n=1571) had incident plaque at the second visit. Compared to those with no to moderate fibrosis, those who had cirrhosis or severe cirrhosis had higher risks of plaque progression with a hazard ratio (HR, 95% CI) of 1.8 (1.1-2.9, P=0.026), and of incident plaque with a HR (95% CI) of 2.6 (1.5-4.6, P=0.0009), adjusted for sex, smoking, hypertension, albuminuria, LDL-C, and HDL-C. Similar results were found among participants with intermediate fibrosis scores. Conclusions: The prevalence of HSI-defined NAFLD is high in AI. NAFLD fibrosis score predicts both incident and progressive carotid atherosclerosis.

Objective To analyze the differences of body composition and islet function between patients with or without nonalcoholic fatty liver disease (NAFLD), and between patients with or without visceral obesity in type 2 diabetes mellitus (T2DM). The effects of fatty liver and visceral fat on islet function were also investigated. Methods A total of 519 patients with T2DM were divided into 4 groups according to the presence or absence of fatty liver and visceral obesity. Group 1: 242 cases of T2DM+ NAFLD with visceral obesity, group 2: 59 cases of T2DM + NAFLD without visceral obesity, group 3: 101 cases of T2DM with visceral obesity but without NAFLD and group 4: 117 cases of T2DM without NAFLD and visceral obesity. Bioelectrical impedance method was used to analyze human body composition, including visceral fat area, skeletal muscle content, mineral content and other indicators. At the same time, biochemical indicators such as liver and kidney function, blood lipid, oral glucose tolerance and islet function were measured in all patients. Variance analysis or nonparametric test was used to compare the difference of body composition and biochemical indexes between groups. Spearman rank correlation was used for correlation analysis, and binary logistic regression was used for multivariate analysis. Results (1)The mineral content, protein content, total body water, body mass index in group 1 were higher than those in group 4 (F=16.202-100.482, all P<0.05); the percentage of fat was decreased gradually from group 1 to group 4 (T=47.027, P<0.05); the skeletal muscle content in group 2 was higher than that in group 1 (T=2.879, P<0.05). (2)The white blood cell, C-reactive protein, total protein, albumin, gamma glutamyl transferase, alanine aminotransferase, aspertate aminotransferase, estimated glomerular filtration rate, serum uric acid, triglyceride, low-density lipoprotein-cholesterol and very low-density lipoprotein-cholesterol showed a downward trend, and the level of high density lipoprotein-cholesterol was increased gradually (F/T=4.036-18.831, all P<0.05) from group 1 to group 4. (3)Among the four groups, homeostatic model assessment of insulin resistance, homeostasis model assessment of β cell function, insulin sensitivity index, area under curve of insulin and area under curve of C-peptide showed a downward trend from group 1 to group 4, with significant difference between group 1 and group 4 (F/T=5.757-13.860, all P<0.05). (4)After adjusting for age and sex, the visceral fat area was positively correlated with body mass index, waist to hip ratio, visceral fat content, subcutaneous fat content, basal metabolic volume, gamma glutamyl transferase, alanine aminotransferase, aspertate aminotransferase and serum uric acid(r=0.340-0.916, all P<0.05), and negatively correlated with high density lipoprotein-cholesterol(r=-0.442, P<0.05). (5)Visceral fat content(OR=5.463, 95% CI: 1.886-4.451, P=0.071)and low-density lipoprotein-cholesterol (OR=1.224, 95% CI: 1.180-1.227, P=0.025)were independent risk factors for NAFLD in patients with T2DM. Conclusions Both T2DM patients with NAFLD or visceral obesity have insulin resistance and compensatory increase of insulin secretion. The most serious insulin resistance is found in T2DM patients with NAFLD and visceral obesity simultaneously. Increasing skeletal muscle content is beneficial to control visceral obesity and improve islet function in patients with NAFLD. Reducing visceral fat area is beneficial to improve metabolic indicators. Key words: Type 2 diabetes mellitus; Non-alcoholic fatty liver disease; Visceral obesity; Body composition; Insulin resistance

Background: Type 2 diabetes mellitus has been linked with abnormal liver function tests. Increased activities of liver enzymes such as aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), ?-glutamyl transferase (GGT) are markers of liver cell injury. Increased activity of these markers is associated with metabolic syndrome, insulin resistance and type 2 diabetes mellitus. This study was aimed to evaluate the significance of liver enzymes such as aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), ?-glutamyl transferase (GGT) in type 2 diabetes mellitus patients. Materials & Methods: Total of 108 cases of type 2 diabetes mellitus patients, comprising of 68 males (62.9%) and 40 females (37%) were included in the study. 110 healthy subjects were includes as controls. Age of the subjects ranged between 27 to 75 years. Serum sample was used for the estimation of study parameters such as FBS, PPBS, AST, ALT, ALP, GGT, Total bilirubin, Direct bilirubin, Total proteins and Albumin. Results: In the present study, mean values of AST, ALT, ALP and GGT were statistically significantly increased in type 2 diabetes mellitus patients when compared to controls (P value 0.001). Conclusion: In this study, we found an association between the increased levels of liver enzymes such as AST, ALT, ALP and GGT in type 2 diabetes mellitus patients. Increased levels of ALT and AST are the surrogate markers for associated non alcoholic fatty liver disease in type 2 diabetes mellitus patients. Hence, testing for AST, ALT, ALP, and GGT should be carried out to screen for underlying non alcoholic fatty liver disease (NAFLD) in type 2 diabetes mellitus patients.

Non-alcoholic fatty liver disease (NAFLD) has become one of the most common forms of chronic liver disease worldwide and its prevalence is expected to continue rising. NAFLD has traditionally been considered a consequence of metabolic syndrome (MetS). However, the link between NAFLD and MetS components, especially type 2 diabetes mellitus (T2DM), hypertension (HTN), and cardiovascular disease (CVD) is more complex than previously thought. Indeed, the adverse effects of NAFLD extend far beyond the liver, with a large body of clinical evidence now suggesting that NAFLD may precede and/or promote the development of T2DM, HTN and atherosclerosis/CVD. The risk of developing these cardiometabolic diseases parallels the underlying severity of NAFLD. Accumulating evidence suggests that the presence and severity of NAFLD is associated with an increased risk of incident T2DM and HTN. Moreover, long-term prospective studies indicate that the presence and severity of NAFLD independently predicts fatal and nonfatal CVD events. In this review, we critically discuss the rapidly expanding body of clinical evidence that supports the existence of a bi-directional relationship between NAFLD and various components of MetS, particularly T2DM and HTN, as well as the current knowledge regarding a strong association between NAFLD and CVD morbidity and mortality. Finally, we discuss the most updated putative biological mechanisms through which NAFLD may contribute to the development of HTN, T2DM and CVD.

The role of specific adipokines in the formation of adipose tissue dysfunction is considered. Obesity is a multifactorial disease that is characterized by excessive adipose tissue accumulation in the body and is a risk factor for the development of several other diseases, including type 2 diabetes mellitus, cardiovascular diseases, and non-alcoholic fatty liver disease. Obesity is one of the main causes of chronic diseases and disability in modern society. Adipose tissue takes an active part in cellular reactions and metabolic homeostasis and does not represent inert tissue only for energy storage. In obesity, excessive accumulation of visceral fat causes adipose tissue dysfunction, which greatly contributes to the occurrence of concomitant diseases. Adipose tissue is capable of synthesizing and releasing a large number of hormones, cytokines, extracellular matrix proteins, growth factors, and vasoactive factors, which are collectively called adipokines, affecting various physiological and pathophysiological processes in the body. Perivascular adipose tissue produces cytokines that affect angiogenesis and peripheral vascular resistance. Adiponectin suppresses the production of glucose in the liver and enhances fatty acid oxidation in the skeletal muscles, which together contribute to a favorable metabolic effect in energy homeostasis, protect cells from apoptosis, and reduce inflammation in various cell types through receptor-dependent mechanisms. Leptin modulates vasoconstriction depending on sympathetic activity while resistin is involved in insulin resistance due to inflammation, wherein its high level determines metabolically unhealthy obesity. Additionally, visfatin plays an important role in the pathogenesis of vascular inflammation in obesity and diabetes mellitus while osteopontin regulates the production of inflammatory mediators by immune cells and omentin plays an important anti-inflammatory and insulin-sensitizing role. The production of most inflammatory mediators in adipose tissue dysfunction increases and contributes to the progression of obesity and related metabolic and vascular disorders. Considering adipokines as biological markers of pathological processes is necessary since their study will create prerequisites for preventive measures and will contribute to the positive treatment process.

Objective To investigate the prevalence and risk fatcors of nonalcoholic fatty liver disease (NAFLD) and its relationship with albuminuria in in-patients with type 2 diabetes mellitus (T2DM).Methods A total of 1 205 in-patients with T2DM were enrolled in this study.The patients were divided into NAFLD group and nonNAFLD group by mean of liver uhrasonography,and into negative albuminuria group (NA) and albuminuria group (AU) according to albumin-to-creatinine ratio.The general information and laboratory data of patients were collected.Chi-square test and binary logistic regression analysis were conducted.Results (1) The prevalence of NAFLD in the patients with T2DM was 60.8％.Binary logistic regression revealed that NAFLD was positively correlated with triglyceride,body mass index (BMI),fasting plasma glucose,waist circumference,diastolic blood pressure,and systolic blood pressure (SBP),and negatively correlated with serum creatinine,duration of diabetes,AU,and high density lipoprotein-cholesterol (HDL-C,all P＜0.05).(2) The prevalence of AU was 31.0％ in these patients.Binary logistic regression revealed that AU was positively correlated with total cholesterol (TC),HbA1C,BMI,duration of diabetes,SBP,and creatinine; and negatively correlated with NAFLD and HDL-C (all P ＜0.05).(3) As subjects were divided into three groups based on their age,the prevalence of NAFLD was decreased and that of AU was increased with aging and diabetes duration (all P＜0.05).The prevalence of NAFLD in patients with AU was significantly lower than that in patients without AU (53.4％ vs 64.2％,P＜0.05).Partial correlations analysis indicated no significant correlation between NAFLD and AU after being adjusted by age and duration of diabetes(P＞0.05).Conclusions With aging and prolonged diabetes,the prevalence of NAFLD is decreased and that of AU is increased.NAFLD is negatively correlated with AU,but this correlation does disappear after adjustment for age and duration of diabetes. Key words: Diabetes mellitus, type 2; Nonalcoholic fatty liver disease; Albuminuria

<h3>Background</h3> Type 2 Diabetes Mellitus (T2DM) is a comorbidity commonlycomorbidity related to fatty liver and a recently proposed definition of ‘metabolic associated fatty liver disease’ (MAFLD) is thought to be a better encapsulation of fatty liver compared to non-alcoholic fatty liver disease (NAFLD). Yet, despite the significant prevalence of fatty liver amongst T2DM patients, current literature has focused on the general implications of a name change without specify to T2DM patients and the impact of the change in definition in T2DM patients remains limited. Hence, we sought to examine the outcome differences between MAFLD(+)/NAFLD(-) and MAFLD(+)/NAFLD(+) in T2DM patients. <h3>Methods</h3> The current study uses open-source data from the United States National Health and Nutrition Examination Survey (NHANES) from 1999 to 2018. Fatty liver was retrospectively diagnosed with a fatty liver index ≥60. The 3 groups in the analysis were T2DM patients without fatty liver [MAFLD(-)/NAFLD(-)], T2DM in MAFLD and NAFLD [MAFLD(+)/NAFLD(+)] and T2DM in MAFLD but not NAFLD [MAFLD(+)/NAFLD(-)]. Multivariate survival analysis was conducted with a cox regression and sub-distribution hazard ratio for competing risk events. <h3>Results</h3> A total of 6,727 patients were included and 4982 individuals with T2DM had fatty liver. 2032 were MAFLD(+)/NAFLD(-) and 2,950 patients were MAFLD(+)/NAFLD(+) (IDDF2022-ABS-0126 Figure 1). The change in definition resulted in a 68.89% increase in fatty liver diagnosis. Compared to MAFLD(+)/NAFLD(+), MAFLD(+)/NAFLD(-) were at a higher risk of adverse events including MACE, advance fibrosis, all-cause (IDDF2022-ABS-0126 Figure 2) and cardiovascular-related mortality. In MAFLD(+)/NAFLD(-), viral hepatitis was a major predictor of advance fibrosis (OR: 6.77, CI: 3.92 to 11.7, p&lt;0.001) and all-cause mortality (HR: 1.75, CI: 1.29 to 2.40, p&lt;0.001). <h3>Conclusions</h3> T2DM patients are predisposed to developing fatty liver and the change in definition allows for the inclusion of all hepatic steatosis in T2DM under MAFLD. However, there were significant differences in the outcomes of the patients between MAFLD(+)/NAFLD(-) and MAFLD(+)/NAFLD(+), and there remains much heterogeneity within the included population of MAFLD.

Non-alcoholic fatty liver disease (NAFLD) is a common disorder and its prevalence is expected to increase due to the rising incidence of type 2 diabetes mellitus (T2DM) and obesity. NAFLD is associated with increased mortality rates and cardiovascular disease is the leading cause of death in these patients. The pathogenesis of NAFLD is not completely elucidated but insulin resistance and oxidative stress appear to play a major role. NAFLD is more prevalent and more severe in patients with T2DM. A multitude of pharmacological agents have been evaluated in NAFLD but most studies were small, short-term and yielded unsatisfactory results in terms of efficacy. Patients with T2DM and NAFLD appear to be even less responsive to the evaluated agents. Thus, the optimal management strategy for NAFLD remains unclear. On the other hand, preliminary data suggest that lifestyle intervention can reduce the incidence of NAFLD in overweight or obese patients with T2DM. Accordingly, prevention of obesity and T2DM is of paramount importance for the reduction of the prevalence of NAFLD and of its associated cardiovascular and liver-related complications.

Background: Type 2 diabetes mellitus (T2DM) patients potentially are at risk of developing non-alcoholic fatty liver disease (NAFLD), Non-alcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disease in developing and developed countries, Global prevalence of NAFLD is 25.24% with highest prevalence in the Middle East and South America and lowest in Africa.Aim of Study: This study aimed to determine the prevalence of NAFLD among T2DM patients, diagnosed by ultrasonog-raphy of liver, to study the age, sex in NAFLD and to compare liver enzymes and lipid profile between individuals with NAFLD and without NAFLD.Patients and Methods: A prospective study was conducted of 100 type 2 diabetic Patients visited a private clinic in Aden republic of Yemen, in the period from October 2017 to June 2018.Results: Total of (100 patients) type 2 diabetes mellitus ambulatory patients were selected for the study. 62 patients (62%) had NAFLD and 38 patients (38%) had normal liver on ultrasonography, the prevalence of NAFLD in the present study was 62%, Majority of the study population observed with type 2 diabetes mellitus and NAFLD were females (n=40, 65%), and 22 were males (35%), the age range of diabetic patients with NAFLD was 40-65 years, mean age 53.16 SD ±7.64, Subjects with diabetes mellitus and NAFLD had sig-nificant elevation in Alanine transaminase (ALT), cholesterol, LDL, and triglyceride than diabetic subjects without NAFLD.Conclusions: Early detection and optimum control of diabetes mellitus is important to minimize the effect of diabetes on liver. Hence, assay of serum levels of hepatic enzymes, and abdominal ultrasound to detect NAFLD should be done in all patients with T2DM as preliminary diagnostic tests.

Obesity is a chronic metabolic inflammatory disease caused by energy excess, characterized by excessive adipose tissue accumulation, and is often accompanied by multiple complications such as type 2 diabetes mellitus, metabolic-associated fatty liver disease (MAFLD), and neurological disorders. Adipose tissue plays a central role in maintaining energy homeostasis. Under conditions of energy excess, pro-inflammatory M1-type adipose tissue macrophages (ATMs) are activated, secrete inflammatory factors, inhibit lipolysis and thermogenesis pathways, and exacerbate metabolic disorders. Insulin-like growth factor 2 (IGF2) possesses both metabolic and immunomodulatory functions and is associated with obesity risk; however, its role in ATM polarization remains unclear. This study aims to clarify the regulatory role and mechanism of IGF2 in obesity-related metabolic inflammation and cognitive function. A high-fat diet (HFD)-induced obese mouse model was established, and interventions were performed via intraperitoneal injection of recombinant IGF2 (rIGF2). Phenotypic polarization of ATMs and expression of inflammatory factors were analyzed by quantitative polymerase chain reaction (qPCR) and immunofluorescence staining. Western blotting was used to detect the expression levels of key proteins in the adrenergic signaling pathway and molecules related to lipolysis/thermogenesis in adipose tissue. Changes in the expression of hippocampal synaptic proteins and cognitive function were evaluated by Western blotting and cognition-related behavioral tests. The study found that rIGF2 intervention significantly promoted the polarization of ATMs from the pro-inflammatory M1 type to the anti-inflammatory M2 type, reduced the levels of inflammatory factors such as tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1), thereby relieving the inhibition of the β-adrenergic signaling pathway, activating the expression of hormone-sensitive lipase (HSL) and uncoupling protein 1 (UCP1), promoting lipolysis and thermogenesis, and effectively improving metabolic abnormalities such as insulin resistance and hepatic steatosis in obese mice. Meanwhile, rIGF2 treatment upregulated the expression of synaptic proteins (e.g., PSD-95, Synapsin-1) in the hippocampus of obese mice and significantly ameliorated HFD-induced cognitive impairment. This study is the first to systematically clarify the dual mechanism of IGF2 in regulating ATM polarization to improve metabolic inflammation, lipolysis-thermogenesis balance, and central cognitive impairment in obesity. The results suggest that IGF2 is not only a key regulator of energy metabolism but also possesses immunomodulatory and neuroprotective potential, providing a new theoretical basis and potential therapeutic target for the prevention and treatment of obesity and its related complications.

Non-alcoholic fatty liver disease (NAFLD) is a disease characterized by a steatosis of the liver that may progress to more serious pathological conditions including: nonalcoholic steatohepatitis (NASH), fibrosis, and cirrhosis. As the prevalence of NAFLD has increased worldwide in recent years, pathophysiology and risk factors associated with disease progression of NAFLD are at the focus of many studies. NAFLD is related to and shares common serum biomarkers with cardiovascular disease (CVD), type 2 diabetes mellitus (T2DM), obesity, and metabolic syndrome (MetS). West Virginia (WV) is a state with some of the highest rates of CVD, obesity and diabetes mellitus. As NAFLD is closely related to these diseases, it is of particular interest in WV. Currently there is no cost-effective, standardized method used clinically to detect NAFLD prior to the onset of reversible complications. At this time, the diagnosis of NAFLD is made with costly radiologic studies and invasive biopsy. These studies are only diagnostic once changes to hepatic tissue have occurred. The diagnosis of NAFLD by traditional methods may not allow for successful intervention and may not be readily available in areas with already sparse medical resources. In this literature review, we identify a list of biomarkers common among CVD, T2DM, obesity, MetS and NAFLD. From this research we propose the following biomarkers are good candidates for inclusion in a panel of biomarkers for the early detection of NAFLD: adiponectin, AST, ALT, apo-B, CK18, CPS1, CRP, FABP-1, ferritin, GGT, GRP78, HDL-C, IGF-1, IL-1β, 6, 8, 10, IRS-2PAI-1, leptin, lumican, MDA SREBP-1c and TNF-α. Creating and implementing a biomarker panel for the early detection and attenuation of NAFLD, prior to the onset of irreversible complication would provide maximum benefit and decrease the disease burden on the patients and healthcare system of WV.

Background: Non-alcoholic fatty liver disease (NAFLD) is the most common cause of liver disorders worldwide. Regarding the shortage of evidence on NAFLD in type 1 diabetes mellitus (T1DM) and the importance of a thorough assessment of complications due to childhood diseases, this study aimed to assess the need for the early detection of NAFLD in children with T1DM. Methods: This cross-sectional study was conducted on 234 children with T1DM referred to 17 Shahrivar Hospital, Rasht, Iran. This study also assessed demographic characteristics, medical history, physical examination, laboratory tests, and hepatic ultrasound. The Mann-Whitney U and chi-square tests were used to compare the children with and without NAFLD. Additionally, univariate and multivariate logistic regressions were used to determine the predictors of NAFLD. Results: This study was conducted on 235 children with T1DM with a median age of 11.0 years (interquartile range (IQR): 8.0 - 14.0) and diabetes duration of 2.0 years (IQR: 1.0 - 4.0). The prevalence of NAFLD was estimated to be 10.2%. The children with NAFLD were significantly older (P = 0.016) and had a larger waist circumference (WC) z-score (P = 0.008) than those without NAFLD. Multiple logistic regression analyses showed that the odds of NAFLD increased with rising age (odds ratio (OR) = 1.29, 95% confidence interval (CI): 1.09 - 1.52) and WC z-score (OR = 2.39, 95% CI: 1.49 - 3.84). The cut-off point for the WC z-score was -0.025 (sensitivity = 58.3%, specificity = 72.0%). Conclusions: The NAFLD frequency in T1DM is relatively low (10.2%) and mainly consists of grade I fatty liver. The NAFLD screening should be further noticed in T1DM children with increasing age and WC as the predictors of NAFLD.

The relationship between nutrient intake, lifestyle, and non-alcoholic fatty liver disease in patients with type 2 diabetes mellitus: Results from the National Health and Nutrition Examination Surveys 2007-2018.