Sorry this got complicated, I tried to put the genetic bit simply but it's hard to do it and after spending a long time on it . I wasn't sure about posting it. Please ignore if too much!
Family history of diabetes, overweight, unhealthy diet, physical inactivity, increasing age, high blood pressure, ethnicity, impaired glucose tolerance. History of gestational diabetes, and poor nutrition during pregnancy. These are considered the major risk factors by the IDF.
Researchers investigate what translates these risks into developing the condition from many different perspectives; exercise, diet, psychology, biochemistry, genes etc .
Putting findings together into a cohesive whole is difficult (impossible?) and people find new facets every day.
There is no one, simple answer, it's one big jigsaw (or maybe lots of big jigsaws)
Fat cells , specifically overfilled fat cells resulting in fat being deposited where it shouldn't be is thought to play a big part in why people become insulin resistant. I wrote briefly about it here:
http://www.diabetes.co.uk/forum/threads/guarantee-diabetes.60294/#post-575102)
. Just to show how complicated, this one aspect is: here is a whole technical book about the role of fat cells in T2 (and though I know a bit, most of it is way above my head)
http://www.intechopen.com/books/role-of-the-adipocyte-in-development-of-type-2-diabetes
Genes
There are specific gene mutation like those involved in MODY or
the cyclist in this article ( He has very few fat cells, that's why he's thin and why fat becomes deposited in the wrong places resulting insulin resistance and T2 like diabetes). I'm sure that more of these specific mutations will be found.
For most , genes play just a part . People may have genetic variations that lead to bit less insulin being secreted than others or to fewer fat cells or to less efficient signalling between cells or some other differences in metabolism.
Twin studies have found T2 to be about 26% heritable (in European populations, it may be higher/lower in other ethnic groups, we don't know) .
http://www.snpedia.com/index.php/Heritability
This means that though about a quarter of the variation between those who have it or don't have it may be influenced by genetic difference, the other 75% of variation is influenced by environment .
There is a gene/environment interaction.
There have been over 40 genetic variations ( ie SNPS) found so far , Each individual variation only increases the risk of developing T2 by a tiny amount. Someone with a lot of these genetic variations would have a higher risk of diabetes than someone with only a few but it seems by not very much.
The four graphs here show those who developed diabetes over a period of 10 years.
The graphs are shown in increasing order of genetic risk., the graph on the left shows results from people with the lowest genetic risk, the one on the right the group with people at the highest risk.
The black lines show those with a BMI of 30 and above, the blue lines BMI of 25 but less than 30 , the red lines those with a BMI of less than 25.
If you look at the red line (BMI under 25) in each graph, you will see that even in the highest risk group there is only a slight increase in those that developed diabetes.
If you look at the black line (BMI over 30) in each graph , you will see that these people had a higher risk of getting diabetes even when they were in the lowest risk group with only a small number of 'diabetes gene variations' (caveat has to be known variations , if there is a genetic variation that has a huge influence, it's not been found yet,)
The study found that younger, leaner people with many of the genes had a higher risk of developing diabetes than those that had only a few . However,
this was in real terms a low risk. So basically, with the genes we know about so far, they only have a very small influence on whether people develop diabetes or not
http://www.plosmedicine.org/article/info:doi/10.1371/journal.pmed.1001647
(
these findings are not applicable to people of other ethnic origins, only people with European ancestry. The data sets were European , and a very big sample including the UK, they looked at 49 SNPs )
Epigenetic changes which is where genes and the environment meet.
Epigenetic changes are not a change in the DNA but a change in the way inherited DNA is bound up . How tightly or loosely sections of DNA is bound up and folded determines whether the code at that section can be read and acted on.
Really excellent
diagram here
Epigenetic changes can arise in the womb and be transmitted to offspring.
Studies in mice have shown that the grandmothers diet can effect the tendency of her grandchild towards obesity The male mice from mothers who were starved at the end of pregnancy were of small birthweight and prone to be glucose intolerant. The male offspring of these mice were in turn prone to be glucose intolerant. ( lots of research going into the different epigenetic markers that may 'cause' this.)
http://epigenome.eu/en/1,63,0
Dutch famine and effects
http://www.naturalhistorymag.com/features/142195/beyond-dna-epigenetics)
Epigenetic changes to DNA also take place during the life of people so may for example influence the expression of the genes that are involved in insulin production
http://www.eurekalert.org/pub_releases/2014-03/lu-ecc030714.php