Heterogeneity of IR-GIP in Normal Subjects and Insulin-Dependent Diabetics

2015 ◽  
pp. 167-174
Author(s):  
T. Krarup ◽  
J. J. Holst ◽  
K. Lindorff Larsen ◽  
S. Madsbad
Keyword(s):  
Normal Subjects ◽  
Insulin Dependent

Urinary Beta-Thromboglobulin Correlates with Impairment of Renal Function in Patients with Diabetic Nephropathy

1986 ◽  
Vol 56 (02) ◽  
pp. 229-231 ◽  
Author(s):  
A H Hopper ◽  
H Tindall ◽  
J A Davies
Keyword(s):  
Renal Function ◽  
Diabetic Nephropathy ◽  
Microvascular Disease ◽  
Normal Subjects ◽  
Specific Protein ◽  
Creatinine Concentration ◽  
Β2 Microglobulin ◽  
Plasma Creatinine Concentration ◽  
Insulin Dependent ◽  
Indium 111

SummaryTBeta-thromboglobulin (βTG) is a platelet-specific protein and since its concentration in plasma rises when platelets are activated, it has been used as an indicator of platelet involvement in vascular disease. Since platelets might be involved in the pathogenesis of diabetic microvascular disease we measured urinary βTG in 20 insulin-dependent diabetics with nephropathy and compared the results with those from 20 normal subjects. Measurement of βTG in urine was undertaken to avoid errors induced by blood sampling and to gain information over a prolonged period using a single assay. Measurements were made of βTG, β2-microglobulin and total protein in urine collected for 24 h and creatinine and β2 microglobulin in plasma. Survival of indium-111-labelled platelets was measured in nine patients. Urinary PTG was significantly (p <0.02) increased in the 20 patients compared with 20 normal volunteers (median value 1.3 vs 0.8 μg/24 h). There was a strong correlation between urinary βTG excretion and plasma creatinine concentration (r = 0.8, p <0.0001) and plasma β2-microglobulin concentration (r = 0.9, p <0.0001). Urinary βTG concentration did not correlate with platelet survival. The results indicate that although urinary βTG is significantly increased in patients with diabetic nephropathy its concentration in urine correlates with indicators of glomerular filtration rather than with a test of platelet activation.

Response of plasma somatostatin-like immunoreactivity (SLI) to a 75 g oral glucose tolerance test in normal subjects and patients with impaired glucose tolerance

1983 ◽  
Vol 104 (4) ◽  
pp. 468-474 ◽  
Author(s):  
Mitsuyasu Itoh ◽  
Yoshifumi Hirooka ◽  
Noriyuki Nihei
Keyword(s):  
Diabetes Mellitus ◽  
Glucose Tolerance ◽  
Human Peripheral Blood ◽  
Normal Subjects ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Oral Glucose ◽  
Insulin Dependent ◽  
Somatostatin 14

Abstract. To study the role of somatostatin in the pathophysiology of glucose intolerance in man, plasma somatostatin-like immunoreactivity (SLI) was measured in 8 normal subjects, 6 patients with insulin dependent diabetes mellitus (IDDM), 13 with non-insulin dependent diabetes mellitus (NIDDM), and 9 with hyperthyroidism, by extraction of plasma SLI and radioimmunoassay. The extraction method gave a recovery rate for synthetic somatostatin-14 and somatostatin-28 of 72 ± 6 and 55 ± 7%, respectively. No SLI corresponding to somatostatin-28 in human peripheral blood was observed. Incubation of somatostatin-28 in plasma gave a rapid decrease of immunoreactivity, and no conversion to somatostatin-14 was observed. It is speculated that SLI extracted with acid-acetone mainly represents a molecular weight similar to somatostatin-14. After oral administration of glucose (75 g), a clear and sustained rise in plasma SLI was seen in normal subjects from an initial value (± sem) of 29.9 ± 5.4 pg/ml to a peak value, at 60 min of 93.4 ± 15.5 pg/ml. The increase of plasma SLI after 75 g glucose was also observed in IDDM and NIDDM. The peak level of SLI was significantly less than that for normal subjects. The extraction of plasma SLI with acetic acid and acetone gave reproducible results and showed a fluctuation of SLI with glucose concentration.

Impaired sodium excretion in response to volume expansion induced by water immersion in insulin-dependent diabetes mellitus

1986 ◽  
Vol 71 (4) ◽  
pp. 403-409 ◽  
Author(s):  
J. P. O'Hare ◽  
J. M. Roland ◽  
G. Walters ◽  
R. J. M. Corrall
Keyword(s):  
Normal Control ◽  
Volume Expansion ◽  
Water Immersion ◽  
Normal Subjects ◽  
Diabetic Group ◽  
Dependent Diabetes Mellitus ◽  
Renal Response ◽  
Control Subjects ◽  
Fractional Excretion Of Sodium ◽  
Insulin Dependent

1. The renal response to volume expansion produced by water immersion to the neck at 35°C was examined in eight young normotensive uncomplicated insulin-dependent diabetic subjects and in eight matched normal control subjects. 2. Both the diabetic and normal subjects manifested a renal response of natriuresis and kaliuresis on immersion, but the natriuretic response was reduced in the diabetic group. Thus the induced excretion of sodium over the 4 h of immersion was 40 ± 5 mmol (mean ± sem) in the normal group compared with 22 ± 4 mmol in the diabetic group (P < 0.02). 3. In the normal subjects creatinine clearance did not change during immersion compared with pre-immersion control values while in the diabetic group it rose from pre-immersion control values of 112 ± 11 ml/min to a mean value of 127 ± 11 ml/min during immersion (P < 0.01). 4. The diabetic subjects thus excreted less sodium despite an increased filtered load during water immersion. Fractional excretion of sodium was significantly reduced in the diabetic subjects compared with the normal control subjects (P < 0.05). 5. The suppression of plasma renin and aldosterone was similar in normal and diabetic groups. 6. Tubular sodium retention could be an early functional change in the diabetic kidney, and be implicated in the development of diabetic nephropathy.

Serum Immunoreactive Trypsin in Tropical Pancreatic Diabetes Syndrome

1989 ◽  
Vol 26 (1) ◽  
pp. 69-73 ◽  
Author(s):  
C S Yajnik ◽  
A Katrak ◽  
S V Kanitkar ◽  
S S Naik ◽  
V D'Souza ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Biochemical Marker ◽  
Normal Subjects ◽  
Β Cell ◽  
C Peptide ◽  
Pancreatic Diabetes ◽  
Immunoreactive Trypsin ◽  
Insulin Dependent ◽  
Tropical Pancreatic Diabetes

Fifteen patients with tropical pancreatic diabetes syndrome (TPDS), 16 insulin-dependent diabetics (IDD), 27 non-insulin-dependent diabetics (NIDD) and 14 normal subjects, all from India, were investigated for markers of β-cell (C-peptide) and exocrine (immunoreactive trypsin; IRT) reserve. IRT and C-peptide concentrations were the lowest in TPDS, lower than normal in IDD, and not significantly different from normal in NIDDs. There was a highly significant correlation ( rs = 0·;D93; P < 0·;00001) between IRT and C-peptide (measured in 50% of patients and controls) concentrations when all diabetic groups were combined. Such a correlation was absent when TPDS patients were considered in isolation, largely because of the markedly low IRT concentration. Fourteen of 15 patients (93%) with TPDS had subnormal IRT concentrations, of which 11 had IRT values of less than 50 μg/L. These IRT values are similar to those previously reported in cystic fibrosis. Only 6 of 16 IDDs (38%) had subnormal IRT concentrations, of which only one was below 50 μg/L. These data suggest that exocrine pancreatic reserve is markedly diminished in TPDS and that a subnormal IRT concentration may be a useful biochemical marker for this form of diabetes.

Relationship between the Basal Blood Alanine Concentration and the Removal of an Alanine Load in Various Clinical States in Man

1980 ◽  
Vol 58 (4) ◽  
pp. 301-309 ◽  
Author(s):  
M. Elia ◽  
Vera Ilic ◽  
Susan Bacon ◽  
D. H. Williamson ◽  
R. Smith
Keyword(s):  
Metabolic Response ◽  
Physiological State ◽  
Normal Subjects ◽  
The Body ◽  
Diabetic Patients ◽  
Adequate Diet ◽  
Insulin Dependent ◽  
Cirrhotic Patients ◽  
Lactate And Pyruvate ◽  
Insulin Dependent Diabetic

1. Blood alanine was measured in six patients undergoing total hip replacement and in four normal subjects starved for 4 days. Hypoalaninaemia occurred in both groups and persisted in the surgical patients despite an adequate diet. The blood alanine was also low in four insulin-dependent diabetic patients and in four patients with muscular dystrophy; it was normal in four patients with cirrhotic liver disease. 2. The removal of an intravenous l-alanine load (12 g; 133 mmol) was significantly increased after surgery and in the diabetic patients, unaltered by starvation, and decreased in the cirrhotic patients. 3. Increases in blood glucose were observed when alanine infusion was performed 6 h after surgery and after 3 days' starvation. Increases in blood lactate and pyruvate always occurred after alanine infusion but were most marked 6 h after surgery. 4. These results show that the metabolic response to an alanine load and the ability of the body to remove it alter with change in physiological state, and that the hypoalaninaemia after surgery and in diabetes is related to an increased removal of intravenous alanine, whereas that during starvation is not.

Collagen-Platelet Aggregation in Diabetics. Inhibition by Aspirin (ASA)

1979 ◽  
Author(s):  
C. Luceti ◽  
E.S. Sack
Keyword(s):  
Salicylic Acid ◽  
Platelet Aggregation ◽  
Acid Concentration ◽  
Normal Subjects ◽  
Individual Variations ◽  
Insulin Dependent ◽  
Salicylic Acid Concentration

Platelet aggregation induced by progressive concentratiuna of collagen was performed In 8 Insulin-dependent diabetlce, inmadlately befara and 90 minutes after the Ingestion of 0.500 g ASA. Simultaneously, aarum ASA-estarase activity and plasmatic salicylic acid levels uere Investigated. The results uere compared ulth s previous study performed in 40 normal subjects. (Throb Hasmaat 36:65B, 1976. Contrarlly to the wide Individual variations in platelet reapaneiveneee to collagen round in normal subjecte, diabetlce responded to collagen Lilthin narrow limite Further, diabetica exhibited both algniflcent increased response to collagen end reduced Inhibition by ASA. Also both. ASA-eetereies activity and plasmatic salicylic acid concentration uere slgniflcantly higher In diabetics. A positive correletion uas Found between the minimal collagan concantretlon required to Initiate aggregation pre-ASA and the ASA-lndkiced Inhibition In the aggregation provoked by the highest colleger! concentration. No correlation uee found betusan tha mlnlmel emount of collegen required Fur lnltietlng aggregetlon pre- and pnat-ASA. Our reeults suggest that cullsgen-lnducsd pletelet aggragetlon in dlebetlcs is Inhibited by ASA, but, at varlence with tha results found in normale, euch Inhibition is not releted to the pre-ASA platelet rasponee to collegen.

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