No, unless you include a needle biopsy followed by morphometric measurements and extrapolation from there... but even in that case, pancreatic needle biopsies are not a recommended procedure for routine or even infrequent measurements, and to make matters worse, a needle biopsy will always be far less than quantitative owing to the fact that it is a hit or miss type of a thing when you are looking for something that normally constitutes only about 1-5% of the tissue mass.

Beta cell function is the only reliable parameter that you can measure.

I suggest this link:

https://labnodes.vanderbilt.edu/resource/view/id/3067

Beta cell function is the only reliable parameter that you can measure.

Most of the pathophysiology of diabetes relates t functional impairment, so there a huge overlap between reduced beta cell mass with reasonably preserved function and preserved beta cell mass with profound impairment. The bariatric surgery model is an example of how apparently helpless cases of diabetes may turn into complete remission. I suggest this article: 

Metabolism. 2014 Oct;63(10):1217-27. doi: 10.1016/j.metabol.2014.05.012. Epub 2014 Jun 11.

β-Cell function in type 2 diabetes.

Ferrannini E1, Mari A2.

Abstract

Different in vivo tests explore different aspects of β-cell function. Because intercorrelation of insulin secretion indices is modest, no single in vivo test allows β-cell function to be assessed with accuracy and specificity comparable to insulin sensitivity. Physiologically-based mathematical modeling is necessary to interpret insulin secretory responses in terms of relevant parameters of β-cell function. Models can be used to analyze intravenous glucose tests, but secretory responses to intravenous glucose may be paradoxical in subjects with diabetes. Use of oral glucose (or mixed meal) data may be preferable not only for simplicity but also for physiological interpretation. While the disposition index focuses on the relationship between insulin secretion and insulin resistance, secretion parameters reflecting the dynamic response to changing glucose levels over a time frame of minutes or hours--such as β-cell glucose sensitivity--are key to explain changes in glucose tolerance and are largely independent of insulin sensitivity. Pathognomonic of the β-cell defect of type 2 diabetes is a reduced glucose sensitivity, which is accompanied by normal or raised absolute insulin secretion rates--compensatory to the attendant insulin resistance--and impaired incretin-induced potentiation. As β-cell mass is frequently within the range of nondiabetic individuals, these defects are predominantly functional and potentially reversible. Any intervention, on lifestyle or with drugs, that improves glucose tolerance does so primarily through increased β-cell glucose sensitivity. So far, however, no intervention has proven unequivocally capable of modifying the natural course of β-cell dysfunction.

http://www.ncbi.nlm.nih.gov/pubmed/25070616