Pancreas, cells

A solution to the problem of introns is to isolate mRNA extracted from the human pancreas cells that make insulin. These cells are rich in insulin mRNA from which introns have already been spliced out. Using the enzyme reverse transcriptase it is possible to convert this spliced mRNA into a DNA copy. This copy DNA (cDNA), which carries the uninterrupted genetic information for insulin can be cloned. Although yeast cells (Saccharomyces) can splice out introns it is normal practice to eliminate them anyway by cDNA cloning. 

Fig. 4. The effect of gemcitabine on dNTP pools in human pancreas cells. Pane-1 and BxPC-3 cells were exposed for 2-24 h to 100 or 10 nM, respectively. Cells were then assessed for intracellular dNTP pools. From ref. 21.

The ability of adult stem cells to become something other than what they were destined to be is controversial. One team of scientists has reported that a particularly promising adult stem cell, isolated from bone marrow and called a multipotent adult progenitor cell (MAPC), appears able to develop into many different kinds of specialized cells in the laboratory. Other scientists have not been able to reproduce these results. Additionally, scientists have reported that stem cells found in fat can become muscle cells, nerve cells, or even pancreas cells able to make insulin, under the right laboratory conditions. 

In their report the researchers describe a culturing technique that can turn mouse embryonic stem cells into cell clusters that resemble pancreatic islets. The clusters inner cells produced insulin, while outer cells produced glucagon and somatostatin, two other proteins typically synthesized by pancreatic cells. Most important, the embryonic stem cell-derived pancreas cells produce insulin in response to glucose, the fundamental role of beta cells that regulate insulin secretion. The major shortcoming of the system at this time is the low levels of insulin production. Refinements in culture technique or drug manipulation may be needed to achieve therapeutic levels. 

Type 1 diabetes is a polygenic disease (different genes contribute to its expression) it can be dominant, recessive or intermediate. The gene IDDMl, located in the MHC class II region on chromosome 6, is believed to be responsible for the histocompatibility disorder characteristic of type 1 diabetes. Insulin-producing pancreas cells (/8-cefls) display improper antigens to T-ceUs,... 

In addition in the pancreas cells of alloxan-treated rats we observed the decreasing in the activity of key antioxidative enzymes namely SOD and glutathione peroxidase (Figure 13). 

We detected also that the antioxidative enzymes activity in the pancreas of rats which are susceptible to alloxan-induced diabetes is significantly lower than in pancreas cells of guinea pigs which are very resistant to diabetogenic action of alloxan (Figure 14). 

It seems unavoidable to conclude that high level of antioxidative enzymes activity in pancreas cells of guinea pigs is a cause of resistance of this kind animals to diabetogenic... 

Figure 14. The activity of key antioxidative enzymes (superoxide dismutase and glutathione peroxidase) in pancreas cells of animals which are susceptible (rats) or are resistant (guinea pigs) to diabetogenic action of...

Brain Pancreas -cells Islets Islet cells... 

Communication Hormones are messenger molecules that carry signals from one part of the body to another. Some hormones are proteins. Insulin, a familiar example, is a small (51 amino acids) protein hormone made by pancreas cells. When insulin is released into the bloodstream, it signals body cells that blood sugar is abundant and should be stored. 

The first isolation of an active OST complex, composed of three subunits (ribo-phorin I and II, and OST48) succeeded from dog pancreas cells [17]. The ribo-phorins had been characterized earlier as possible receptors for ribosomes and thought to be involved in protein translocation [119-121]. Since OST activity could be depleted from detergent solubilized extract by anti-ribophorin I antibodies, it became clear that ribophorins are indeed constituents of OST [17], They are no longer believed to be involved in ribosome binding, but in accord with the co-translational nature of A-glycosylation, the identification of ribophorins as part of the OST may indicate a close location of the enzyme to the protein translocation channel. 

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