Abstract.The renin-angiotensin system (RAS) has been unequivocally implicated as a mediator of diabetic complications. The present study was designed to evaluate the RAS in non-insulin dependent diabetic patients with diabetic nephropathy.Plasma renin activity, plasma angiotensin II and serum angiotensin-converting enzyme (ACE) activity were measured in 45 non-insulin dependent diabetes mellitus (NIDDM) patients and 15 healthy non-diabetic controls. Diabetics were subdivided into 15 normoalbuminuric NIDDM subjects, 15 NIDDM patients with microalbuminuria and 15 diabetics with macroalbuminuria. Mean plasma renin activity for macroalbuminuric diabetics (0.65 ±0. 10 ng/ml/hr) was significantly reduced than the controls (1.28 ±0.37 ng/ml/hr) (P < 0.001), the diabetic group with microalbuminuria (1.08 ±0.48 ng/ml/hr) (P < 0.05) and normoalbuminuric patients (1 .56 ±0.82 ng/ml/hr) (P<0.001). A significant negative correlation was obtained between serum creatinine and plasma renin activity (r=-0.842, p<0.001) in macroalbuminuric NIDDM patients. Plasma angiotensin II was significantly decreased in non-complicated diabetics compared to healthy controls (4.36± 1.49 pg/ml vs 14.87 ± 3.48 pg/ml respectively, p < 0.001). Non-insulin dependent diabetic patients with nephropathy had significantly higher plasma angiotensin II levels (28.99 ± 5.88 pg/ml) than non-complicated diabetics (p < 0.001). Serum ACE activity was increased in 53.3% of NIDDM patients. All diabetic groups showed increased serum ACE activity (normoalbuminuric NIDDM 114.9 ± 28.3 nmol/min/ml, microalbuminuric NIDDM 127.9 ± 31.2 nmol/min/ml and macroalbuminuric NIDDM 127.0±29.3 nmol/min/ml) when compared to the normal control group (76.3±16.5 nmol/min/ml) (p<0.001). No significant difference in serum ACE activity was obtained between normoalbuminuric and nephropathic diabetics or between diabetics with and without retinopathy.No significant correlation was obtained between serum ACE activity and blood pressure, blood glucose level and duration of diabetes. Thus plasma renin activity is decreased in diabetic nephropathy and negatively correlates with serum creatinine. Plasma angiotensin II is decreased in normoalbuminuric diabetics and elevated in diabetic nephropathy. Serum ACE activity is raised in NIDDM patients with no relation to albumin excretion rate. The role of increased ACE activity in NIDDM remains to be established.
Glucagon hormone being catabolic and hyperglycemic, it acts in an opposite manner to insulin and adds to insulin resistance. The oligosaccharide inulin fructans is indigestible in the small bowel. When it reaches the large intestine, it encourages beneficial microbacteria strains. These latter produce certain peptides which when absorbed they reach the endlocrine L-cells of the small gut. These peptides stimulate L-cells to release glucagon like peptide 1 (GLP-1) which suppresses glucagon and stimulates insulin secretion in a glucose dependant manner. Our aim is to find how inulin suppresses glucagon and to what extent this improves insulin resistance. Fasting serum glucagon and homeostasis model assessment for insulin resistance (HOMA-IR) were estimated in 28 type 2 diabetic female patients before and after twenty one days of daily inulin intake. Fasting serum glucagon and HOMA-IR decreased significantly after the inulin intake period. In conclusion inulin stimulates the release of GLP-1. This acts in a glucose dependant manner thus simulating the novel incretin based drugs in reducing insulin resistance. However, owing to inulin other actions on insulin resistance, it might exceed these novel drugs.
Systemic inflammation describes certain metabolic alterations which are mediated by inflammatory cytokines. Theses occur essentially as a defensive body response towards offending agents such as surplus nutrient staffs. Our aim is to find out the role of inulin as a protective agent against metabolic inflammation. Twenty eight type 2 diabetic females were subjected to the estimation of their serum high sensitivity C-reactive protein, lipopolysaccharides, tumor necrosis factor alpha, adiponectin and HOMA-IR test before and after three weeks of inulin ingestion. There was a significant drop in the level of serum high sensitivity C-reactive protein, lipopolysaccharides, tumor necrosis factor alpha, HOMA-IR and a non-significant rise in serum adiponectin after inulin ingestion. In summary inulin can act as a useful protective agent in systemic inflammation.
Type 2 diabetic microangiopathy affects every organ in the body and can lead to serious incapacitating complications. VLDL and apo C1 are two of the main biochemical abnormalities which start and propagate this condition. Inulin fructans prebiotic effect on the colonic flora enhance the bifidogenic strains. These predominate over the pathogenic strains which encourage lipidogenesis, thus reducing hyperlipidemia. Our aim is to find out the possible effect of inulin ingestion on the metabolism of VLDL and apo C1 and their role in the pathogenesis of diabetic angiopathy Twenty eight obese type 2 diabetic female patients were subjected to this study. Each patient ingested 4 grams of inulin daily for 3 weeks. Their fasting serum level of VLDL and apo C1 were estimated before and after the period of inulin ingestion. There was a significant decrease in fasting level of serum VLDL and apo C 1 after inulin ingestion period. In conclusion inulin can be given as a protective and as an add on therapy for type 2 diabetic patients. It reduces two of the main culprits which start and propagate the pathologic pathway of diabetic microangiopathy. This cuts short the other offenders (small HDL, small dense LDL and the small VLDL remnants).
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