Are the fat induced histological changes in liver reversible ?

Dear Mohd Saleem Itoo

The accumulation of fats in the liver (liver steatosis "LS") causes variable damage in hepatocytes

The most common cause of LS is metabolic syndrome (MS), simple obesity or associated MS and DM2.

LS causes alteration in the function of hepatocytes and visualization under microscope and within the hepatocytes, of fat microvesicles in a nearby area and around the perivenular veins and minimal degree of inflammation:

In grade I or incipient LS, histological changes can be stopped or reversed if the metabolic alteration that induces such changes is controlled or eliminated, such as MS and Hyperlipidemia control, weight loss in Obesity and adequate control of DM2.

Failing to prevent or controlling the inducing factors of LS-GI, the condition evolves to a greater degree of fat infiltration and inflammatory changes; That is, to Steatohepatitis. In this case, with a good therapeutic control of the factors related to aggravation, in the best case, the changes can be reversed to a lower degree of LS.

To continue and not to decrease the Steatohepatitis, areas of fibrosis appear histologically (healing by cicatrization of inflammatory areas). That is, it is histologically identified the maximum degree of intracellular fat infiltration and areas of fibrosis interspersed with zones of inflammation around the central vein of the lobules (Perivenular). Alterations similar to those observed in alcoholism, except for the accumulation of fat. This grade of histological lesion is irreversible in 80% of the cases, frequently leading the majority to the final stage of Liver Cirrhosis.

http://www.scielo.org.co/scielo.php?script=sci_arttext&pid=S0120-99572014000100012

regards

Jose Luis

Estimado Mohd Saleem Itoo

La acumulación de grasas en el hígado (esteatosis hepática "EH") ocasionan daño variable en los hepatocitos

La causa más común de EH es el síndrome metabólico (SM), la obesidad simple o asociada el SM y DM2.

La EH ocasiona alteración en la función de los hepatocitos y visualización bajo microscopio y dentro de los hepatocitos, de microvesículas de grasa en una área cercana y alrededor de las vénulas (perivenular) y grado mínimo de inflamación:

En la EH grado I, o incipiente, los cambios histológicos pueden detenerse o revertirse si se controla o se elimina la alteración metabólica que induce tales cambios, como sería control del SM e Hiperlipidemia, bajar de peso en la Obesidad y control adecuado de DM2.

De no prevenir o controlar los factores inductores de HE-GI, evoluciona el cuadro a un grado mayor de infiltración grasa y cambios inflamatorios; es decir, a Esteatohepatitis. En este caso, con un buen control terapéutico de los factores relacionados del agravamiento, en el mejor de los casos, se pueden revertir los cambios a un grado menor de EH.

De continuar y no disminuir la Esteatohepatitis, histológicamente aparecen zonas de fibrosis (curación por cicatrización de áreas inflamatorias). Es decir, histológicamente se identifica grado máximo de infiltración grasa intracelular y areas de fibrosis intercaladas con zonas de inflamación alrededor de la Vena Central de los lobulillos (Perivenular). Alteraciones similares a las que se observan en el alcoholismo, excepto por la acumulación de grasa. Este grado de lesión histológica es irreversible en el 80% de los casos, llevando con frecuencia a la mayoría al estado final de Cirrosis Hepática.

http://www.scielo.org.co/scielo.php?script=sci_arttext&pid=S0120-99572014000100012

Saludos

José Luis

Joachim Pimiskern

Here are studies that appear to be related.

http://www.hopkinsmedicine.org/news/media/releases/obesity_induced_fatty_liver_disease_reversed_in_mice

https://phys.org/news/2012-12-scientists-compound-reverses-fatty-liver.html

https://source.wustl.edu/2014/06/fatty-liver-disease-prevented-in-mice/

http://www.scripps.edu/news/press/2012/20121219burris.html

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0075980

https://www.eurekalert.org/pub_releases/2012-04/uoic-uoi042012.php

http://www.news-medical.net/news/2008/10/14/41999.aspx

https://www.eurekalert.org/pub_releases/2015-02/uog-pcm022515.php

https://www.eurekalert.org/pub_releases/2016-11/w-dae112116.php

https://www.eurekalert.org/pub_releases/2012-02/w-ccr020212.php

Regards,

Joachim

Julian Schulze zur Wiesch

1. That is the hope

http://journals.lww.com/md-journal/Fulltext/2016/06070/Nonalcoholic_fatty_liver_disease_is_associated.42.aspx

2. To a certain Point/degree the changes are reversible-

3. there is a Point of no return

Hailemichael Desalegn Mekonnen

Mostly we are considering the steatosis from either metabolic syndrome in overweight/obese, type 2 DM patients. The steatosis can be reversed if they present at an early stage of fibrosis.

The other concern could be patients with fat accumulation after rapid weight loss, lean individuals with steatosis, which might have a genetic predisposition.

What do you think about lean individuals with steatosis? How can we reverse the steatosis?

Here, we can see that it is not simply the fat accumulation, but genetic and other factors including the microbiome need to be altered.

Regards

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