Sameer,

Could you provide a link for the publication in question?

General wisdom holds that Glut4 is expressed in fat and muscle cells. There is some expression of Glut4 in the hippocampus region of brain as well. I am curious to see how and at what level it was detected in the liver.

http://www.proteinatlas.org/ENSG00000181856-SLC2A4/tissue

Sameer,

There was a comment by someone earlier which claimed something to the effect that Glut4 is present in all insulin sensitive organs, mostly liver, adipose, muscle.

In my opinion, the comment was inaccurate. I notice now that the post has been deleted which is for the best.

I asked you to post the source of information to note the technique and sensitivity of detection - use of sensitive technique without distinction of morphological location of signal could mislead a person in making wrong conclusions. For example, smooth muscle cells express Glut4. SMCs are present in blood vessels. If mRNA is measured by a sensitive enough method, one may see the signal in highly vascularized organs such as the liver. However, it does not mean that hepatocytes (or Kuppfer cells) express Glut4. If sections of liver are carefully analyzed by in situ hybridization, my guess is that one would find signal for Glut4 along the blood vessels.

Hi Sameer. As you well know, GLUT-4 is insulin-regulated and it's present only in skeletal and cardiac muscle, adipose tissue. Although liver tissue is insulin-sensitive, do not presents glut-4 but only glut-2 (and glut-7), and the reason is that the liver uptakes and releases glucose, and glut-2 can works bilaterally, facilitating glucose transit from interstitial liquid to the cell and vice versa, while glut-4 not. Moreover, glut-2 isn't saturable, has low affinity (high Km), high capacity and facilitates the transit of other monosaccharides  such as fructose. Liver tissue also has Glut-7 which allows the intracellular transport. 

So for the liver tissue it's much better to have glut-2 than glut-4, although it is insulin-sensitive.

Best regards,

FM

paper title

Gallic Acid Regulates Body Weight and Glucose Homeostasis Through AMPK Activation

in figure 2 or 3 (L)

http://press.endocrine.org/doi/abs/10.1210/en.2014-1354?journalCode=endo

Tausif Alam

the correct figure:

Figure 3 L    rt-PCR results (liver tissue)

Thank Vero but I checked the website, GLUT4 mRNA in liver is extremely very low compared to that in skeletal muscle and adipose tissue

Sameer,

The figure shows increase in Glut4 mRNA as a result of Gallic acid treatment. In extracting RNA from liver tissue, all the blood vessels within the liver will also be present.

As I mentioned earlier, without reliable information about localization of Glut4 (for example by immunocytochemistry or in situ hybridization), given the historical information about Glut4, it is unreasonable to claim that Glut 4 is present in hepatocytes.

I have never detected GLUT4 expression in liver but only in muscle and fat cells. As indicated by others, if any GLUT4 expression occurs in the liver, it is very low compared to muscle and fat cells

Thanks for all

Vincent, was your observation based on measurements in the whole tissue homogenates or was it via techniques such as immunocytochemistry or in-situ hybridization where one can ascertain that the presence of Glut4 corresponds to hepatocytes?

What is a glucose transporter connected with insulin receptor in liver then?

In liver is Glut2

In liver cells, it is GLUT2 which is expressed and GLUT4 is expressed at significant level in insulin-sensitive tissues (muscle cells, heart cells, adipoyctes). If there is any detected GLUT4 expression in the liver (depending on the techniques), it will be very low and therefore with no biological significance to my knowledge. This is the important point.

Conditional depletion of GLUT4 in either adipose tissue or skeletal muscle causes insulin resistance and a roughly equivalent incidence of diabetic animals (Zisman et al., 2000 and Abel et al., 2001). This was particularly surprising in the former case since adipose tissue accounts for only a small fraction of total body glucose disposal (James et al., 1985). These tissue-specific depletions of GLUT4 have profound metabolic effects on other tissues. For example, mice with muscle-specific GLUT4 deficiency display decreased insulin responsiveness in adipose tissue and liver (Zisman et al., 2000), while those with adipose-specific GLUT4 depletion exhibit muscle and liver insulin resistance (Abel et al., 2001).

http://www.sciencedirect.com/science/article/pii/S1550413107000678

Glut2 is insulin independent. So I ask what is insulin receptor for in liver? Is it GSK3 that it trigers? And what kind of glucose transport then?

Dear Abu-Eid,

One more paper that might be of interest to you - liraglutide upregulated liver and muscle GLUT4 in KKay mice.

https://www.spandidos-publications.com/10.3892/ijmm.2013.1453

Best,

Jan

Hi, I am running some WB and ELISAs of primary mouse hepatocytes and I could detect GLUT4 in membrane fraction by both WB and ELISA. will try to run immunofluorescence to confirm. Looks like it is there but in low amounts.

Any update on this?

No, Glut4 is only expressed in the skeletal and adipose tissue while glut2 is expressed in the pancreas.

Thank you.

glut2 express in pancreas and liver

Thank you, bc I could find it in the liver hepatocytes membranes.

Glut4 mRNA expression in rat is present in Stellate cells of the liver parenchyma. Although the protein expression was not observed.

Shinodo et al., 2001. Acta histochemia 34: 15-24.

Thank you, I still see it in the liver in good amounts in the membrane fractions both in WB and ELISA of many mice, wild type and transgenic.