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Biomedical subjects

J H Pinkney

Publications and source records attributed to J H Pinkney.

24 records · Page 2Linked to original sources
PubMed1995

The relationship of urinary albumin excretion rate to ambulatory blood pressure and erythrocyte sodium-lithium countertransport in NIDDM.

Increased erythrocyte sodium-lithium countertransport rate is found in non-diabetic subjects with essential hypertension, and in insulin-dependent diabetic subjects with nephropathy. However, relationships between these variables in non-insulin-dependent diabetic subjects are ill-defined. In order to characterise the relationships between blood pressure, urinary albumin excretion, and erythrocyte sodium-lithium countertransport, 66 subjects with non-insulin-dependent diabetes were studied. Urinary albumin excretion rate correlated with mean 24-h ambulatory systolic blood pressure (r = 0.57; p < 0.001), but not with sodium-lithium countertransport (r = 0.06; p = 0.31). No significant relationship was observed between 24-h systolic blood pressure and erythrocyte sodium-lithium countertransport (r = 0.16; p = 0.17). The principal differences between microalbuminuric and normoalbuminuric subjects (albumin excretion rate > 15 micrograms.min-1 [n = 20], and < 15 micrograms.min-1, [n = 46]) were: higher 24-h systolic blood pressure (145.9 [16.8] mmHg vs 131.9 [16.8] mmHg; p = 0.006), nocturnal heart rate (72.4 [8.9] vs 67.4 [8.9] beats.min-1; p = 0.042), and HbA1 (11.3 [1.5]% vs 10.1 [2.0]%; p = 0.028), and a longer median duration of diabetes (10.0 vs 5.0 years; p = 0.02). In contrast, there was no significant difference in sodium-lithium countertransport rate between microalbuminuric (0.41 [0.18] mmol.l-1.h-1) and normoalbuminuric subjects (0.39 [0.15] mmol.l-1.h-1; p = 0.687).(ABSTRACT TRUNCATED AT 250 WORDS)

Age of Onset↗
PubMed1995

Insulin resistance and not hyperinsulinaemia determines erythrocyte Na+/Li+ countertransport in non-insulin-dependent diabetes mellitus.

Insulin resistance and increased erythrocyte Na+/Li+ countertransport activity are well documented in subjects with essential hypertension, raising the question whether compensatory hyperinsulinaemia might be responsible for activating Na+/Li+ countertransport. We measured Na+/Li+ countertransport in 63 non-nephropathic non-insulin-dependent diabetic subjects (36 hypertensive, 27 normotensive), finding no correlation with fasting levels of insulin (r = 0.074, P = 0.28), despite using a sensitive and specific insulin assay. In contrast, in 33 of the subjects in whom insulin sensitivity was measured, Na+/Li+ countertransport correlated significantly with the whole body glucose clearance rate (r = -0.37, P = 0.036). It is concluded that increased Na+/Li+ countertransport may be a cellular marker for insulin resistance, but that hyperinsulinaemia is not likely to be the factor which mediates this relation.

Aged↗
PubMed1994

Insulin resistance, insulin, proinsulin, and ambulatory blood pressure in type II diabetes.

Both insulin resistance and insulin concentrations correlate with blood pressure in nondiabetic subjects, but there is no consensus on these relations in subjects with non-insulin-dependent diabetes, perhaps because of the use of nonspecific insulin assays and clinic blood pressure measurement. Therefore, we have investigated the relation between ambulatory blood pressure, insulin sensitivity (measured by an insulin sensitivity test), and levels of insulin and its principal precursors, measured by specific assays, in 24 subjects with non-insulin-dependent diabetes. Insulin sensitivity (glucose metabolic clearance rate) correlated strongly with mean 24-hour ambulatory systolic blood pressure (r = -.650, P < .001). In contrast, there was no relation between this blood pressure index and fasting levels of insulin (r = .096, P = NS) or all insulin-like molecules (r = .077, P = NS). Dichotomized on 24-hour ambulatory systolic blood pressure levels, the hypertensive group was more insulin resistant than the normotensive group (metabolic clearance rate, 3.6 [0.7] versus 6.5 [3.0] mL.kg-1.min-1, P = .006), whereas there was no difference in insulin or proinsulin concentrations among the groups. In multiple regression analysis, insulin sensitivity was the major determinant of blood pressure. We conclude that in subjects with non-insulin-dependent diabetes mellitus, blood pressure is related to insulin sensitivity but not to fasting levels of insulin, suggesting that hyperinsulinemia is probably not the mediator of this relation.

Ambulatory Care↗
PubMedDate not supplied

Insulin resistance in non-insulin-dependent diabetes mellitus is associated with microalbuminuria independently of ambulatory blood pressure.

Microalbuminuria in both insulin-dependent (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM) is a marker for insulin resistance. Microalbuminuria is also associated with hypertension, itself an insulin-resistant state. Therefore, in order to examine the independent relationships of microalbuminuria with blood pressure and insulin resistance, we measured ambulatory blood pressure (Takeda TM-2420), insulin resistance (modified Harano method), and urinary albumin excretion rate (overnight urine collection) in 36 subjects with NIDDM. Albumin excretion correlated with 24-h systolic blood pressure (r = 0.49, p = 0.003), and insulin sensitivity (r = -0.39, p = 0.007). Microalbuminuric subjects had reduced insulin sensitivity compared with normoalbuminuric subjects [Mean (SD) 2.95 (0.33) versus 4.67 (0.56) ml.kg-1.min-1; p = 0.013]. In multivariate analysis including ambulatory blood pressure and insulin resistance, urinary albumin excretion was associated primarily with insulin resistance, with smaller contributions from glycated hemoglobin and male gender. These data suggest that microalbuminuria in NIDDM, although associated with hypertension, is also independently associated with insulin resistance.

Albuminuria↗