Educational panel illustrating the macroscopic and microscopic pathology of Nonalcoholic Steatohepatitis (NASH) in a mouse model. Panel A presents the gross anatomy of dissected control and model mice. Panel B provides a high-resolution clinical photograph comparing a healthy control liver (dark red/brown, smooth surface) with a NASH model liver (pale yellow-tan, suggestive of steatosis and atrophy). Panel C displays diagnostic histopathology using Hematoxylin and Eosin (H&E) staining at 100x and 400x magnifications. The control group micrographs show normal hepatocyte architecture with organized cords and clear sinusoidal spaces. In contrast, the NASH model micrographs demonstrate hallmark features of hepatic steatosis, including diffuse macrovesicular and microvesicular fat deposition, hepatocyte ballooning, and cellular disarray. The 400x magnification specifically highlights large, clear vacuoles within the cytoplasm of hepatocytes, which displace the nuclei to the periphery. This comparison serves as a diagnostic reference for metabolic liver disease research and pathological classification.

This composite of abdominal MRI scans and quantitative data illustrates advanced hepatic pathology, specifically nonalcoholic steatohepatitis (NASH). Panels (a) and (b) show T1-weighted In-Phase and Opposed-Phase images, demonstrating a significant drop in signal intensity across the liver parenchyma in the opposed-phase image, a hallmark of diffuse fatty infiltration (steatosis). Panel (c) provides quantitative 'LiverLab' analysis, indicating a proton density fat fraction (PDFF) of 26.3% (moderate-to-severe steatosis) and an effective R2* of 55.1 s⁻¹, ruling out significant iron overload. Panels (d) and (e) compare an unenhanced T1 Vibe sequence with a Hepatobiliary Phase (HBP) image following gadoxetic acid administration. The HBP image reveals a failure of the liver to enhance relative to the kidneys, signaling severely impaired hepatocyte uptake and advanced liver dysfunction consistent with fibrosis. This sequence of images serves as a clinical diagnostic tool for assessing chronic liver disease by combining morphologic fat quantification with functional hepatobiliary assessment.

Educational visual showing the progression of Non-Alcoholic Steatohepatitis (NASH) to Hepatocellular Carcinoma (HCC) through gross and microscopic pathology. Panels A-C are clinical photographs of liver specimens from a research model, displaying distinct polyp-like, exophytic tumor growths (blue arrows) on a reddish-brown liver surface. Panel D-F show Hematoxylin and Eosin (H&E) stained sections at various magnifications (scale bars: 40 μm and 100 μm). The histology reveals a clear transition margin (black arrows) between noncancerous parenchyma and the malignant tumor. Key histopathological features include a trabecular growth pattern of atypical hepatocytes, significant macrovesicular steatosis (lipid vacuoles), inflammation, and clusters of hyperchromatic nuclei. This comparison illustrates the typical morphological changes and architectural distortion seen in NASH-associated liver cancer, highlighting the diagnostic criteria for differentiating steatotic liver tissue from neoplastic growth.

This composite image presents a preclinical study of nonalcoholic steatohepatitis (NASH) using a zebrafish model (LmiR21). Section A displays gross clinical photographs comparing livers from control (LmiR21-Dox) and experimental (LmiR21+Dox) groups at 6 months post-fertilization (mpf). In both males and females, the miR-21 induced livers (+Dox) appear enlarged, pale red, and greasy, consistent with hepatomegaly and steatosis. Section B provides histopathological analysis using Masson’s trichrome staining. The control liver (B1) shows normal hepatic architecture and cellularity. In contrast, the miR-21 overexpressing liver (B2) exhibits hallmark NASH phenotypes, including extensive hepatocyte ballooning (a), increased Mallory-Denk bodies (b, arrows), and significant lobular inflammation (c, d, arrows). These histopathological features demonstrate the progression from simple steatosis to steatohepatitis and early fibrosis, evidenced by blue-stained collagen deposition. This image serves as a translational model for understanding the role of microRNA-21 in hepatic lipid metabolism, inflammation, and fibrogenesis.