Hi David,
there is only one study.

Here is the original abstract :

http://www.ncbi.nlm.nih.gov//entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citat
ion&list_uids=16377570

Dietary and genetic control of glucose transporter 2 glycosylation promotes
insulin secretion in suppressing diabetes.

Ohtsubo K, Takamatsu S, Minowa MT, Yoshida A, Takeuchi M, Marth JD.

Howard Hughes Medical Institute and Department of Cellular and Molecular
Medicine, 9500 Gilman Drive, University of California, San Diego, La Jolla,
CA 92093, USA.

Pancreatic beta cell-surface expression of glucose transporter 2 (Glut-2) is
essential for glucose-stimulated insulin secretion, thereby controlling
blood glucose homeostasis in response to dietary intake. We show that the
murine GlcNAcT-IVa glycosyltransferase is required for Glut-2 residency on
the beta cell surface by constructing a cell-type- and glycoprotein-specific
N-glycan ligand for pancreatic lectin receptors. Loss of GlcNAcT-IVa, or the
addition of glycan-ligand mimetics, attenuates Glut-2 cell-surface
half-life, provoking endocytosis with redistribution into endosomes and
lysosomes. The ensuing impairment of glucose-stimulated insulin secretion
leads to metabolic dysfunction diagnostic of type 2 diabetes. Remarkably,
the induction of diabetes by chronic ingestion of a high-fat diet is
associated with reduced GlcNAcT-IV expression and attenuated Glut-2
glycosylation coincident with Glut-2 endocytosis. We infer that beta cell
glucose-transporter glycosylation mediates a link between diet and insulin
production that typically suppresses the pathogenesis of type 2 diabetes.

PMID: 16377570

Here is one of their most striking tables :
Mgat4a Null mice are the mice where the particular gene has been knocked
out, they miss a gene called GnT-4a

12 Weeks of Age, 8 Weeks on High-Fat

                           Chow Wild-Type      Mgat4a Null

Gluc (fast) (mg/dl)    214.5 ± 21.25    208.9 ± 8.91
Gluc (fed) (mg/dl)     237.4 ± 11.53    307.2 ± 10.45 (p = 0.0001)
Insulin (fast) (ng/ml)  5.838 ± 1.313    2.656 ± 0.551 (p = 0.0423)
Insulin (fed) (ng/ml)   6.617 ± 0.907   4.023 ± 0.324 (p = 0.0123)
Free fatty acid (fast)  1.85 ± 0.09       1.780 ± 0.060
Free fatty acid (fed)  1.59 ± 0.08        1.560 ± 0.060
Triglyceride (mg/dl)  104.3 ± 8.53      98.86 ± 5.53
AST (IU/l)               100.9 ± 7.19      106.0 ± 5.62
ALT (IU/l)               72.50 ± 9.31      84.29 ± 6.87
Lipase (U/l)              64.50 ± 6.70      66.00 ± 7.27
Total chol (mg/dl)     149.2 ± 10.80    171.1 ± 4.70
HDL chol (mg/dl)     122.0 ± 8.49      117.9 ± 5.96
Body weight (g)        39.00 ± 1.90     47.17 ± 2.47 (p = 0.0002)

The fasting glucose is the same , the postprandial Glucose is very different
(p = 0.0001)
The insulin , both fasting (p = 0.0423) and post prandial (p = 0.0123), is
very different
The body weight is very different (p = 0.0002)

So if you fed two types of mice THE SAME FAT DIET only one type , the one
that is missing a very special gene , GnT-4a  , (or has a misfunctioning
GnT-4a  gene) WILL GET DIABETES TYPE II

These findings are consistent with the possibility that the pathogenesis of
type 2 diabetes in response to a high-fat diet may be contingent upon
diminished cell-surface Glut-2 levels due to reduced GnT-4a
activity.Attenuated glucose-transporter expression and loss of GSIS
(glucosestimulated insulin secretion) are characteristic of early pancreatic
b cell dysfunction in multiple manifestations of type 2 diabetes among
humans and rodents, including Zuker diabetic fatty rats,
biobreeding/Worcester diabetic rats, and db/db mice lacking the leptin
receptor (Orci et al., 1990b; Thorens, et al.,1990, 1992; Unger, 1991;
Guerra et al., 2005)

!!!!!!!!! due to reduced GnT-4a activity !!!!!!!!

YOUR GENETIC MAKE-UP WILL CAUSE BOTH THE WEIGHT GAIN AND THE DIABETES

To use your peferred font ....

hth
Gys