I think you're asking what you do to keep IRS-1 and/or IRS-2 from
downregulating.  There's an extensive literature for this.  I don't
regularly follow it but this is what's in my notes.  I suspect
intermittent fasting will also improve insulin sensitivity via IRS-1/2
but I haven't checked.

green tea increase insulin-stimulated glucose uptake and insulin binding
to adipocytes; EGCG mimics insulin by stimulating tyrosine
phosphorylation of the insulin receptor and IRS-1 and increases
phosphoinositide 3-kinase (PI3K), MAPK and p70, EGCG also inhibits
glucose production in the liver, possibly by repressing genes for
gluconeogenesis <http://www.jbc.org/cgi/content/full/277/38/24933>

in obese rats, exercise training along with alpha lipoic acid improves
the skeletal muscle levels of IRS-1 (insulin receptor substrate-1),
glucose transport along with activity of p85 subunit of PI3K [PMID
15068957]

diabetes can be induced by knocking out both insulin receptor substrates
(IRS); low levels of IRS-1 in the liver prompt it to make more glucose
(upregulated gluconeogenic enzymes glucose-6 phosphatase and
phosphoenolpyruvate carboxykinase; also increased hepatic nuclear
factor-4 alpha; decreased glucokinase); low levels of IRS-2 made more
triglycerides (it upregulates SREBP-1c and fatty acid synthase and
increased fat accumulation in the liver); blocking both at the same time
lead to fatty liver disease (hepatic steatosis), glucose intolerance and
insulin resistance, defective Akt activation and Foxo1 phosphorylation
[PMID 15711641]