High prevalence of nonalcoholic steatohepatitis and abnormal liver stiffness in a young and obese Mexican population

Abstract

ObjectiveTo identify nonalcoholic steatohepatitis (NASH) and liver stiffness in Mexican subjects with different body mass index (BMI).MethodsA cross-sectional study was conducted in 505 adults. Risk for NASH was defined as the presence of one or more of the following biochemical and metabolic parameters (BMPs): fasting glucose ≥100 mg/dl, triglycerides (TG) ≥150 mg/dl, homeostatic model assessment of insulin resistance (HOMA-IR) ≥2.5, aspartate aminotransferase (AST) >54 IU/L and alanine aminotransferase (ALT) >42 IU/L. Body mass index measurement and nutritional assessment were performed by standard procedures. Liver fibrosis stage was determined by liver stiffness measurement using transitional elastography (TE) or by liver biopsy (LB).ResultsRisk for NASH was 57% (290/505). Most BMPs values incremented by BMI category. Among 171 at-risk patients, 106 subjects were evaluated by TE and 65 subjects by LB. Abnormal liver stiffness (≥6.0 kPa) was prevalent in 54% (57/106) of the cases, whereas by LB, 91% (59/65) of patients with obesity had NASH and liver fibrosis. Furthermore, liver fibrosis was prevalent in 46% (6/13) in normal weight individuals, whereas 4.6% (3/65) of patients with a BMI ≥ 35 kg/m2 showed no histopathological abnormalities. Overall, 67.8% (116/171) of the patients had abnormal liver stiffness or NASH. The normal weight patients with liver damage consumed relatively a higher fat-rich diet compared to the other groups whereas the remaining subgroups shared a similar dietary pattern.ConclusionYoung patients with overweight and obesity showed a high prevalence of altered BMPs related to abnormal liver stiffness assessed by TE and NASH by LB. Early diagnostic strategies are required to detect the risk for NASH and avoid further liver damage in populations with a rising prevalence of obesity by defining the risk factors involved in the onset and progression of NASH.

<p>Association of Apolipoprotein e2 Allele with Insulin Resistance and Risk of Type 2 Diabetes Mellitus Among an Admixed Population of Mexico</p>

“…Alongside, HOMA-IR values were also altered in both normal weight and overweight subjects who were non-diabetic e2 allele carriers; however, HOMA-IR values were normalized in those who were obese. Notably, this subgroup of patients considered metabolically healthy has been reported previously 30 suggesting that other genes may exert protective effects in these subjects. Nonetheless, in this study, most T2DM patients were obese, a factor that can potentiate the development of IR by increasing the delivery of fatty acids to the liver and muscle exceeding the storage and oxidative capacities of these tissues 37 and by activating enzymes that negatively regulate insulin action.…”

“…29 ALT was increased in obese non-diabetics and was frankly altered in T2DM patients suggesting the onset of liver damage as previously reported in young and obese Mexican subjects with nonalcoholic steatohepatitis and abnormal liver stiffness. 30 In conjunction, these metabolic alterations in the context of obesity are alarming considering the subjects' age and re-enforce the need of national prevention programs to diminish the up rise of mortality in Mexico due to the triad of T2DM, cardiovascular and liver diseases. 31 On the other hand, the effect of ApoE alleles on the serum lipid concentrations has been extensively investigated.…”

Cognition and hospitalizations are linked with salivary and faecal microbiota in cirrhosis cohorts from the USA and Mexico

“…This was performed in cohorts from the USA and Turkey, where the diets are radically different 7 . In this current study, we compared US‐based Western diet to Mexico, which has a unique amalgamation of being a middle‐income country with high obesity and lactose intolerance 9‐11 . All decompensated patients had lower vegetables, animal protein and animal fat intake compared to compensated patients and controls, but this difference was greater within the Mexican cohort.…”

“…This was associated with lower hospitalizations in the Turkish cohort 7 . Cirrhosis is also prevalent in other middle‐income countries in the Western hemisphere, including Mexico, where a genetic predisposition to obesity, a relatively lower socio‐economic status and lactose intolerance give a unique opportunity to study these interactions 9‐11 . The comparison between Mexico and the USA is important because despite their proximity, dietary, genetic and socio‐economic differences can potentially affect gut microbiota and cirrhosis progression.…”

A Regionalized Genome-Based Mexican Diet Improves Anthropometric and Metabolic Parameters in Subjects at Risk for Obesity-Related Chronic Diseases

“…Today, obesity, type 2 diabetes mellitus (T2DM), cardiovascular diseases, dyslipidemias, and non-alcoholic fatty liver disease are highly prevalent in Mexicans related to a nutrition transition, which is shifting the traditional consumption of the ancestral pre-Hispanic diet based on the staple Mesoamerican foods fused with some healthy European ingredients towards an unhealthy hepatopathogenic diet [7,8]. Furthermore, a preceding analysis of DRAG polymorphisms in Mexican populations showed a high prevalence of adaptive alleles (methylenetetrahydrofolate reductase-MTHFR 677T, ATP-binding cassette transporter A1-ABCA1 230C, apolipoprotein E -APOE ε4, and a salivary amylase 1-AMY1 diploid copy number ≥ 6) mainly in NA groups followed by admixed populations (Mestizo) with an intermediate NA ancestry, while a very low frequency of the European lactase-persistence LCT-13910T adaptive allele was observed [9].…”