go for physical slight activity and yoga can prevent deterioration of  beta cells.

That is a question I have asked myself many times. I shall make some proposals though I am planning to test some of them in my PhD too. Firstly, I believe no one mechanism is responsible for beta cell loss, hence no one target will achieve this goal. My hypothesis is that chronic nutritional overload on beta cells is important which results in beta cells activating stress pathways. At this stage, though the beta cells are being stressed, they adapt to stressors (probably by inducing heat shock proteins). This stage I envisage correlates to the compensation stage of beta cell response. With continuous chronic stress, adaptive mechanisms fail and beta cell decompensation occurs. this is evident by production of inflammatory cytokines, induction of apoptosis coupled with age-related decline in proliferative capacity. All these eventually result in beta cell loss. Hence, anti-inflammatory strategies, anti-apoptotic mechanisms might work. Evidence at least from the work of authors like Pedersen BK, Shoelson, Hotamisligil, Donath and a host of others show success of anti-inflammatory strategies (sorry I can't quote their direct papers now). Moreso, recently, role of inter-organ communication is being appreciated. Hence, betatrophin from liver might protect beta cells from death. 

A clear answer to this is what all diabetologists are looking for. Please search in Pubmed to find some answers. Here are some areas which you can explore further:

http://www.betacellsindiabetes.org/betacell-science

http://www.jci.org/articles/view/29103

http://www.diabetesincontrol.com/articles/54-/11534-early-use-of-insulin-to-improve-beta-cell-preservation

Beta cell dysfunction and death is secondary to being overtaxed in the face of insulin resistance where in general the "normal" amount of insulin production and secretion is unable to result in the target glucose levels (euglycemia) - hence, what eventually becomes a redundant and counterproductive cycle of of hyper-production (and secretion) of insulin begins through the initial hypertrophy and hyperplasia of normal beta cells but as the functional insulin insufficiency gets worse, continued efforts of beta cells can't keep uo with the perceived demand of insulin and eventually damage associated with sustained hyperactivity (functional as well as cell proliferative) takes its toll...

Stop or intervene with the root cause of the problem (insulin resistance, metabolic syndrome), the rest will fall in place, hopefully! 

For many people who are obese, losing weight and changing their life style to maintain a normal weight combined with eating balanced multiple meals is already known to help a great deal.

If one is interested in simply protecting beta cells, there is always a possibility of throwing all the known anti-apoptic/oxidative regimen in one's arsenal. At least in the case of experimental rodents, expression of superoxide dismutase makes beta cells sufficiently resistant to oxidative damage that even streptozotocin at conventional concentrations used to induce diabetes does not harm them!

Dear Yongsuo Liu,

The following may satisfy your query

1. Keep the infection/inflammation level low in the blood vessels

2. The central/total obesity level to be checked at regular intervals

3. Involve in the regular physical activity.

4. Over nutrition should be avoided

5. De-stress yourself by spending more time in a place where you feel pleasant and also you may spend more time with kids

Regards,

S.Sivanandam

In a young diabetic between the age 25-35 ,the best option is the exogenous Insulin administration to protect the remaining exhausting beta cells . 

We all know from basic Biochemistry that the autoimmune attack of this beta-cells of the islet of Langerhans is one of the causes of type two diabetes. Therefore any reaction that will inhibit the deregulation of  this destruction of cells will be a crucial therapeutic measure to at least manage the disease state if not to eradicate it.

Induction of some cytokines, MHC proteins and some other proteins involved in the destruction of cells had been linked to this process. Further more, Deregulation of apoptosis due to the impairment of the P53 gene (Tumor suppressor gene) and IAPS (Inhibitor of Apoptosis) may also be involved.

Beta cell loss has no single cause. I believe the putative role of each cause has not been determined in the patients with type 2 diabetes. The causes of beta cell dysfunction include in glucotoxicity, lipotoxicity, inflammation, sulphonylureas, etc.

There is no a single method to stop deterioriation of B cell in typ2 2 diabetes.

First: the degree of damage has to be determined or estimated. Type 2 has a strong inflammatory component and use to be associated with obesity, dislipemia, and other components of the metabolic syndrome.

LOW DAMAGE: when damage is low (eg. in recently diagnosed) it seems that changes in lifestyle (increasing physical activity, diet) may stop the progression of type 2.

HIGH DAMAGE: there are a list of pharmacological interventions that may stop the progress inlcding insulin, GLP-1 agonists, DDP-IV inhibitord etc

Hi,

Just to add-on to the above said comments, negative calorie balance(600 Cal/day) was found to normalise the Beta cell function:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3168743/

The sample size was very low in the above study & Diabetes UK has taken up the project, scaling it up as the largest funded research  project of Diabetes UK currently.

In general, tight glycaemic control & lipid control helps to overcome glucotoxicity and lipotoxicity respectively, thereby helping to restore beta cell function to some extent.

Find the answer and you will be famous! It is generally accepted that people with T2D do better when they begin an intervention (diet, exercise, and/or medication), but after a few years, they begin to decline. Eventually, increased doses are needed and even insulin therapy may be required.

It is generally accepted, at least at this time, that once you start down the path of T2D, you will not be able to return to normoglycemia without pharmacological intervention. But we keep searching for a better way!