Decreased binding of insulin to its receptors in rats with hormone induced insulin resistance

Increased insulin binding by hepatic plasma membranes from diabetic rats: normalization by insulin therapy.

“…Previous studies in which elevated insulin levels are associated with decreased hormonal binding under a variety of conditions (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20) have suggested that the prevailing insulin concentration may itself modulate the number of insulin receptors (13). The present study supports this postulate.…”

“…concentrations in the diabetics were twice as high as those in both the normal controls and patients with pancreatitis. Thus, increased insulin concentrations probably account for the decreased hormonal binding (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20) in these patients. However, purified hepatic plasma membranes from Chinese hamsters (35) and rats2 rendered diabetic with streptozotocin bound approximately twice as much insulin as control membranes, a result in close agreement with our data.…”

“…A decreased capacity for binding insulin is found in hepatic tissue from the ob/ob mouse (1)(2)(3)(4)(5), the db/db mouse (4,5), the normal rat given either gold thioglucose (4) or glucocorticoids (6,7) or harboring a tumor secreting ACTH (8), and the old obese rat compared to young lean animals (9); in monocytes removed from obese humans (10)(11)(12); in cultured lymphocytes (13,14) incubated in vitro in the presence of insulin; in thymocytes (15) and cardiac muscle (16) from the ob/ob mouse; in skeletal muscle from old obese rats compared to young lean animals (17); in adipose tissue from obese humans (12,18), the ob/ob mouse (19), rats given a short course of glucocorticoids (7), and the old obese rat compared to young lean animals (20). Since high levels of insulin in all of these situations are associated with a decreased capacity for binding the hormone, diminished concentrations of insulin might be expected to enhance insulin binding.…”

Insulin antibodies prevent insulin-receptor interactions

“…Insulin initiates its effects by interacting with receptors located on the plasma membrane [1][2][3] and altered insulin receptor interaction may be responsible for hormone resistance [4][5][6][7][8][9][10][11][12][13][14].…”

Dexamethasone‐dependent expression of β1–24 corticotropin stimulated adenylate cyclase during adipose conversion of 3T3‐F442A cells

“…Otherwise glucocorticoid hormones have been shown to have physiological actions on multiple cellular processes; thus, the indirect, so-called 'permissive' actions may involve the modulation of the affinity and/or receptor concentrations of a variety ot ~ heterologous hormone and growth factor receptors [28][29][30][31][32][33][34][35][36][37][38][39][40]. So, given the data presented in this paper, ACTH could regulate its own receptor in adipocytes early during adipose tissue formation via glucocorticoid secretion from the adrenal gland; thus a dual effector mechanism of ACTH action should be retained to render an account of the biological response of the adipose cell to this hormone.…”