Alpha agonists decrease insulin secretion. Therefore, when clonidine, an alpha-2 agonist, is added to the solution, it would decrease the amount of insulin secretion when stimulated with glucose.
Insulin is a 51 amino acid di-peptide (A and B chain) linked by disulfide bonds. It is synthesized in the beta cells of the pancreas as proinsulin (insulin + C-peptide) and is cleaved in the secretory vesicle. When insulin is released, both the c-peptide and insulin are released. Endogenous insulin should contain both insulin and C-peptide; if hyperinsulinemia occurs and similar concentrations of C-peptide are not found, then the insulin is of exogenous origin. Hyperglycemia, growth hormone, cortisol, and beta agonists increase insulin release while hypoglycemia, somatostatin, and alpha agonists decrease insulin release. As in the question, clonidine is an alpha-2 agonist that decreases central adrenergic outflow and is primarily used to treat hypertension but does not decrease blood flow to the kidney.
Nussey and Whitehead discuss the actions of insulin on the liver, adipose tissue, and muscle. Insulin promotes glucose storage via both glycogen synthesis in the liver and also glucose uptake into the muscle and adipose tissue through increasing the number of GLUT4 transporters. The glucose is converted to glycogen in muscle and to fatty acids/triglycerides in adipose tissue.
Wilcox reviews the adrenergic pathway for insulin release. During stress or exercise, catecholamines can inhibit insulin secretion via alpha 2 adrenoreceptors. Although playing a small role, beta adrenoreceptors, when activated, can increase the release of insulin via an increase in cAMP.
Illustration A demonstrates the synthesis of insulin from pre-proinsulin in the ER to proinsulin in the Golgi apparatus to insulin in the secretory vesicle. Illustration B depicts the pathway for insulin release.
Answers 1 & 2: Dobutamine and isoproterenol are beta agonists and would increase the release of insulin.
Answers 3 & 5: Tolbutamide and glyburide are sulfonylureas that increase insulin secretion by closing the potassium channels, resulting in depolarization of the cell and insulin secretion.
Nussey S, Whitehead S. Endocrinology: An Integrated Approach. Oxford: BIOS Scientific Publishers; 2001. Chapter 2, The endocrine pancreas. Available from: http://www.ncbi.nlm.nih.gov/books/NBK30/
Wilcox G. Insulin and insulin resistance. Clin Biochem Rev. 2005 May;26(2):19-39.
PMID:16278749 (Link to Abstract)