Figure 1 - uploaded by Aylin Gökhan
Content may be subject to copyright.
a-c. Normal liver morphology with central vein, wellorganized sinusoids and remark cords. Hepatocytes revealed normal cell shape with centrally placed nucleus and eosinophilic cytoplasm. Normal Kupffer cells. No increase in the connective tissue. Homogeneous staining of normal glycogen distribution. d-f. Disorganized liver architecture. Dilated sinusoids, dispersed remark cords and inflammatory cells infiltration were detected. Fatty degenerations as microvesicular steatosis in the hypertrophic hepatocytes with granular cytoplasm and Kupffer cells are indicated. No significant increase in the connective tissue was confirmed. Presence of glycogen deposition was confirmed by strong positive PAS reaction. g-i. Partially protected liver architecture. Reduced microvesicular steatosis, and hepatocellular hypertrophy. Pronounced inflammatory cells infiltration. Mild activation of Kupffer cells. Scale bar = 20 µm, total magnification 400×. CV: central vein, S: sinusoids, R: remark cords, H: hepatocytes, arrow: Kupffer cells, arrowhead: microvesicular steatosis, asterisk: hepatocellular hypertrophy, star: inflammatory foci.
Source publication
Background:
Nonalcoholic fatty liver is one of the most common forms of liver disease and role of microRNAs (miRNAs) on this illness is currently unclear. It was aimed to evaluate the predictive role of circulating miR-33a and mir-200c on high fructose corn syrup (HFCS)-induced fatty liver and vitamin D3 supplementation-related hepatic changes.
M...
Contexts in source publication
Context 1
... examination of Group 1 slides, stained with H&E, Mallory Trichrome and PAS, normal appearances of the histological structure of liver tissues were observed (Figures 1a-1c). General histological observations consisted of vena centralis located at the center of classical liver lobe, hepatocytes with centralsettled nucleus and eosinophilic cytoplasm, neatly lined remark cords around vena centralis and portal areas, and regular sinusoidal structures. ...
Context 2
... lobules of experimental fatty liver group were disordered. Dispersed remark cords, sinusoidal dilation, inflammatory cell infiltration, hypertrophic hepatocytes filled with multiple fat droplets with central nuclei (microvesicular hepatic steatosis) and hepatocytes filled with large fat droplet with peripheral nuclei (macrovesicular hepatic steatosis) were detected in liver sections of fatty liver group (Figures 1d-1f). NAFLD scores were significantly higher in Group 2 rats. ...
Context 3
... significant connective tissue increase or fibrosis was observed with stained Mallory Trichrome sections in Group 1. Hepatocytes of Group 2 rats were stained by PAS, which indicated the presence of glycogen around the central vein and portal area. Liver architecture integrity of the vitamin D 3 group (Group 3) was partially protected (Figure 1g-1i). A dispersed distribution of hepatocytes with fewer lipid droplets per cell was observed in Group 3. ...
Context 4
... examination of Group 1 slides, stained with H&E, Mallory Trichrome and PAS, normal appearances of the histological structure of liver tissues were observed (Figures 1a-1c). General histological observations consisted of vena centralis located at the center of classical liver lobe, hepatocytes with centralsettled nucleus and eosinophilic cytoplasm, neatly lined remark cords around vena centralis and portal areas, and regular sinusoidal structures. ...
Context 5
... lobules of experimental fatty liver group were disordered. Dispersed remark cords, sinusoidal dilation, inflammatory cell infiltration, hypertrophic hepatocytes filled with multiple fat droplets with central nuclei (microvesicular hepatic steatosis) and hepatocytes filled with large fat droplet with peripheral nuclei (macrovesicular hepatic steatosis) were detected in liver sections of fatty liver group (Figures 1d-1f). NAFLD scores were significantly higher in Group 2 rats. ...
Context 6
... significant connective tissue increase or fibrosis was observed with stained Mallory Trichrome sections in Group 1. Hepatocytes of Group 2 rats were stained by PAS, which indicated the presence of glycogen around the central vein and portal area. Liver architecture integrity of the vitamin D 3 group (Group 3) was partially protected (Figure 1g-1i). A dispersed distribution of hepatocytes with fewer lipid droplets per cell was observed in Group 3. ...
Citations
... A recent study by Tanoglu et al. [148], using a rat model of high-fructose-diet-induced fa y liver, revealed insights into the relationship between vitamin D supplementation and the expression and circulation of microRNAs 200c and 33a. The findings of the study clarified that vitamin D plays a protective role against MASLD, and there was a notable alteration in the circulating levels of miR-200c and 33a associated with vitamin D. Specifically, the results revealed more favorable histopathological alterations in the vitamin-D3-supplemented group including a enuating inflammatory, metabolic, and hepatic effects through miR-33a and miR-200c [148]. ...
... A recent study by Tanoglu et al. [148], using a rat model of high-fructose-diet-induced fa y liver, revealed insights into the relationship between vitamin D supplementation and the expression and circulation of microRNAs 200c and 33a. The findings of the study clarified that vitamin D plays a protective role against MASLD, and there was a notable alteration in the circulating levels of miR-200c and 33a associated with vitamin D. Specifically, the results revealed more favorable histopathological alterations in the vitamin-D3-supplemented group including a enuating inflammatory, metabolic, and hepatic effects through miR-33a and miR-200c [148]. Moreover, within a specific dosage and a defined time frame, vitamin D3 showed the capacity to reduce hepatic lipid accumulation, inflammation, and fa y degeneration induced by high-fructose corn syrup [148]. ...
... The findings of the study clarified that vitamin D plays a protective role against MASLD, and there was a notable alteration in the circulating levels of miR-200c and 33a associated with vitamin D. Specifically, the results revealed more favorable histopathological alterations in the vitamin-D3-supplemented group including a enuating inflammatory, metabolic, and hepatic effects through miR-33a and miR-200c [148]. Moreover, within a specific dosage and a defined time frame, vitamin D3 showed the capacity to reduce hepatic lipid accumulation, inflammation, and fa y degeneration induced by high-fructose corn syrup [148]. These data reinforce the hypothesis that circulating miRNA levels could serve as biomarkers for MASLD [148]. ...
Metabolic dysfunction-associated steatotic liver disease (MASLD) is an increasingly prevalent condition characterized by abnormal fat accumulation in the liver, often associated with metabolic disorders. Emerging evidence suggests a potential link between vitamin D deficiency and the development and progression of MASLD. The current review provides a concise overview of recent studies uncovering novel mechanistic insights into the interplay between vitamin D and MASLD. Several epidemiological studies have highlighted a significant association between low vitamin D levels and an increased risk of MASLD. Vitamin D, traditionally known for its role in bone health, has now been recognized as a key player in various physiological processes, including immune regulation and inflammation. Experimental studies using animal models have demonstrated that vitamin D deficiency exacerbates liver steatosis and inflammation, suggesting a potential protective role against MASLD. Mechanistically, vitamin D appears to modulate MASLD through multiple pathways. Firstly, the vitamin D receptor (VDR) is abundantly expressed in liver cells, indicating a direct regulatory role in hepatic function. Activation of the VDR has been shown to suppress hepatic lipid accumulation and inflammation, providing a mechanistic basis for the observed protective effects. Additionally, vitamin D influences insulin sensitivity, a critical factor in MASLD pathogenesis. Improved insulin sensitivity may mitigate the excessive accumulation of fat in the liver, thus attenuating MASLD progression. In parallel, vitamin D exhibits anti-inflammatory properties by inhibiting pro-inflammatory cytokines implicated in MASLD pathophysiology. Experimental evidence suggests that the immunomodulatory effects of vitamin D extend to the liver, reducing inflammation and oxidative stress, key drivers of MASLD, and the likelihood of hepatocyte injury and fibrosis. Understanding the complex interplay between vitamin D and MASLD provides a basis for exploring targeted therapeutic strategies and preventive interventions. As vitamin D deficiency is a modifiable risk factor, addressing this nutritional concern may prove beneficial in mitigating the burden of MASLD and associated metabolic disorders.
Non-alcoholic fatty liver disease (NAFLD) is a prevalent liver condition that affects people who do not overconsume alcohol. Uncertainties exist over how microRNAs (miRNAs) in the blood and liver relate to NAFLD. The aim of this narrative review was to investigate the role of miRNAs in the onset and progression of non-alcoholic steatohepatitis (NASH) from NAFLD, and explore their potential as diagnostic tools and treatment targets for NAFLD patients. Liver miRNA-34a levels were found to accurately represent the degree of liver damage, with lower levels suggesting more damage. In patients with NAFLD and severe liver fibrosis, higher levels of miRNA-193a-5p and miRNA-378d were found. Moreover, miRNA-34a, miRNA-122, and miRNA-192 levels might aid in differentiating NASH from NAFLD. Similar to this, miRNA-21 and miRNA-27 levels in rats were able to distinguish between steatosis and steatohepatitis. High-fat diets enhanced the expression of 15 distinct miRNAs in rats, and there were substantial differences in the miRNA expression patterns between obese and lean people. The results from the present review imply that miRNA microarrays and sequencing may be helpful diagnostic tools, and miRNAs may be a possible treatment target for patients with NAFLD.
