Increased serum angiotensin converting enzyme activity in type T insulin—dependent diabetes mellitus: its relation to metabolic control and diabetic complications

Abstract

Serum angiotensin-converting enzyme (ACE) was measured in 150 insulin-dependent diabetes mellitus (IDDM) patients and 72 healthy subjects by radioassay, using [3H]-hippuryl-glycyl-glycine as a substrate. Mean (SD) serum ACE activity in diabetic patients was 120 +/- 33 nmol ml-1 min-1 (range 46-215) and was significantly increased by 56% compared to control values (77 +/- 23 nmol ml-1 min-1, range 46-125, P < 0.001). ACE activity > 125 nmol ml-1 min-1 was observed in 60 of 150 IDDM patients. 96 IDDM patients were normoalbuminuric (< 22 mg 24 h-1) and 49 patients were micro- or macroalbuminuric (range 22-6010 mg 24 h-1). Micro- and macroalbuminuric IDDM patients were found to have significantly greater ACE activity values than normoalbuminuric patients (128 +/- 36 vs. 115 +/- 30 nmol ml-1 min-1, P = 0.025). Metabolically well-controlled IDDM patients (glycosylated haemoglobin < or = 8%) had lower ACE activity values than the patients with glycosylated haemoglobin greater than 8% (109 +/- 20 vs. 127 +/- 32 nmol ml-1 min-1, P < 0.02). A significant correlation between degree of metabolic control and ACE activity was found (r = 0.435, P < 0.001) so that an increase in one glycosylated quartile unit is accompanied by an increase in ACE activity of 10.5 nmol ml-1 min-1. Thus ACE activity in the serum of IDDM patients was increased by 56% in 40% of the patients. It was increased in IDDM patients without complications and in patients with retinopathy or nephropathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Involvement of Spinal Angiotensin II System in Streptozotocin-Induced Diabetic Neuropathic Pain in Mice

“…Coppey et al (2006) have shown that treatment with either enalapril, an ACE inhibitor, or L-158809, an AT1 receptor antagonist, prevents or reverses diabetic neuropathy in STZ-induced diabetic rats (STZ rats). Although the evidence indicates that RAS activity is increased in diabetes (Van Dyk et al, 1994;van Dijk et al, 2001), the role of spinal RAS on diabetic neuropathic pain has not been reported to date. Thus, we hypothesized that it was important to examine whether spinal RAS is necessary and sufficient for diabetic neuropathic pain in the STZ mouse model.…”

“…In the diabetic state, there is an increase in plasma ACE activity and levels of Ang II (Van Dyk et al, 1994;van Dijk et al, 2001) and there have been many studies conducted on the relationship between RAS and diabetic complications. One of the outcomes of RAS activation is the hypertrophy of various renal cells promoted by Ang II, which leads to the development of diabetic nephropathy (Leehey et al, 2000;Vidotti et al, 2004).…”

Association between angiotensin-converting enzyme gene polymorphism and diabetic retinopathy in the Chinese population

“…Indeed, previous studies have suggested that high serum levels of ACE were especially associated with PDR. 6 The biological mechanism through which ACE I/D polymorphism may be related to an increased risk of DR is unclear. Serum ACE concentrations are significantly higher in those carrying the D/D genotype than in those carrying the I/D or the I/I genotype.…”

The tissue renin-angiotensin system in human pancreas

“…Interest in the relationship between the systemic RAS and endocrine pancreas function has largely been concerned with the role of Ang II in the the hypertension of diabetes, its complications such as nephropathy, and retinopathy, and their possible control by drugs regulating its action (Hsueh & Anderson 1993, Vandyk et al 1994, Tait & Tait 1997, Goa 1997, Allen 1997, Anderson 1997, Kim et al 1997, Chaturvedi et al 1998. In addition, studies with experimental animals as well as patients have shown that the systemic RAS may be perturbed in diabetes, though the situation is complex, and opposing effects, for example on Ang II receptor function have been reported in different tissues (Sechi et al 1994, Cheng et al 1994, Fliser et al 1997, Brown et al 1997, Nakata et al 1998.…”