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K Hoogenberg

Publications and source records attributed to K Hoogenberg.

46 records · Page 3Linked to original sources

Effect of adiposity on plasma lipid transfer protein activities: a possible link between insulin resistance and high density lipoprotein metabolism.

The mechanisms responsible for the decreased high density lipoprotein (HDL) cholesterol levels associated with obesity and insulin resistance are not well understood. Lecithin: cholesterol acyltransferase (LCAT) and cholesterol ester transfer protein (CETP) are key factors in the esterification of cholesterol in HDL and the subsequent transfer of cholesteryl ester towards apolipoprotein B-containing lipoproteins. Phospholipid transfer protein (PLTP) may be involved in the regulation of HDL particle size. We therefore measured the activities of LCAT, CETP and PLTP using exogenous substrate assays, as well as lipids, lipoproteins, insulin and C-peptide in fasting plasma from eight healthy obese men (body mass index > 27 kg m-2) and 24 non-obese subjects. The obese men had lower levels of HDL cholesterol (P < 0.05) and higher levels of plasma triglycerides (P < 0.05), insulin (P < 0.05) and C-peptide (P < 0.01), as compared to the quartile of subjects with the lowest body mass index (BMI < 22.4 kg m-2). CETP and PLTP activities were elevated in the obese men by 35% (P < 0.01) and by 15% (P < 0.05), respectively. LCAT activity was comparable among the quartiles. Linear regression analysis showed that CETP activity was positively correlated with body mass index (P < 0.02), fasting blood glucose (P < 0.05) and plasma C-peptide (P < 0.05). PLTP activity was positively related to body mass index (P < 0.01), waist to hip circumference ratio (P < 0.001), as well as to fasting blood glucose (P < 0.05) and plasma C-peptide (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Higher plasma lipid transfer protein activities and unfavorable lipoprotein changes in cigarette-smoking men.

The mechanism responsible for the atherogenic lipoprotein changes associated with cigarette smoking are largely unknown. Lecithin: cholesterol acyltransferase (LCAT) and cholesteryl ester transfer protein (CETP) are key factors in the esterification of plasma cholesterol and the transfer of cholesteryl ester from high-density lipoproteins (HDLs) toward very-low- and low-density lipoproteins (VLDLs+LDLs). Another transfer factor, phospholipid transfer protein (PLTP), recently has been shown to be involved in the interconversion of HDL particles in vitro, but its physiological function is not yet clear. We measured the activities of LCAT, CETP (as cholesteryl ester exchange activity), and PLTP using exogenous substrate assays as well as lipoprotein profiles in the plasma of 21 normolipidemic cigarette-smoking men (total plasma cholesterol below 6.5 mmol/L and triglyceride below 2.5 mmol/L) and 21 individually matched nonsmoking control subjects. HDL cholesterol, HDL cholesteryl ester, and plasma apolipoprotein A-I levels were lower in the smokers than in the control subjects (P < or = .05 for all parameters). Median plasma CETP activity was 18% higher (P < .02) and median plasma PLTP activity was 8% higher (P < .05) in the smokers compared with the nonsmokers. LCAT activity was not different between the groups. HDL cholesteryl ester concentration was positively related to LCAT activity in control subjects but not in smokers. By contrast, there was an inverse relation of CETP activity with HDL cholesteryl ester in smokers but not in nonsmokers. Multiple regression analysis demonstrated that the lowering effect of smoking on HDL cholesteryl ester could be explained by its influence on CETP activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Acute pancreatitis in a patient with familial benign hypercalcaemia.

A patient with familial benign hypercalcaemia (FBH) who developed relapsing pancreatitis is presented. She underwent distal partial pancreas resection with surgical removal of pancreatic duct stones, and a pancreaticojejunostomy. No further causes for the pancreatitis were found. The present case is remarkable since it is an example of the occurrence of pancreatitis in a previously known patient with hypercalcaemia, and it underlines the severity of the pancreatitis when it occurs in this syndrome.

Acute Disease↗

Effect of growth hormone and insulin-like growth factor I on urinary albumin excretion: studies in acromegaly and growth hormone deficiency.

Glomerular hyperfiltration is a characteristic feature of acromegaly but it is uncertain whether albuminuria is elevated in this disease. To investigate the role of abnormal growth hormone (GH) and insulin-like growth factor I (IGF-I) levels on urinary protein excretion, we measured the overnight urinary albumin excretion rate (UalbV) and creatinine clearance in 14 acromegalic patients with metabolically active disease (fasting GH > 5 micrograms/l and IGF-I > 2.2 kU/l), 8 GH-deficient patients and 20 control subjects. The UalbV was higher in the acromegalic patients (median 8.4 (range 4.2-68.2) micrograms/min) than in the GH-deficient patients (2.0 (0.9-5.9) micrograms/min, p < 0.001) and control subjects (3.3 (1.0-7.8) micrograms/min, p < 0.01). Five acromegalic patients had UalbV levels above the normal upper normal limit of 10 micrograms/min. Only one patient with concomitant untreated hypertension had persistent microalbuminuria. Creatinine clearance also was higher in the acromegalic patients (p < 0.05) and lower in the GH-deficient patients (p < 0.05) than in the control subjects. In 11 of these acromegalic cases, the lowering of GH by 63% and of IGF-I by 48%, following treatment with the somatostatin analogue (N = 10) or spontaneous pituitary infarction (N = 1), reduced the UalbV by 29% to 4.9 (3.1-45.2) micrograms/min (p < 0.01). Among the acromegalic patients (25 observations), the UalbV was related to GH (r = 0.61, p < 0.01), IGF-I (r = 0.57, p < 0.01) and creatinine clearance (r = 0.54, p < 0.01). In conclusion, circulatory GH and IGF-I levels influence albuminuria.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗

Contributory roles of circulatory glucagon and growth hormone to increased renal haemodynamics in type 1 (insulin-dependent) diabetes mellitus.

The stimulatory effects of growth hormone (GH) and glucagon on renal function are well known, but it is uncertain whether these hormones are involved in the increase in renal function, characteristic of type 1 (insulin-dependent) diabetes mellitus. Therefore, the circulatory levels of GH and glucagon were measured in 10 type 1 diabetic patients with an elevated glomerular filtration rate (GFR > 130 ml min-1 1.73 m-2) and in 20 age and sex matched normofiltering patients (GFR ranging from 90-130 ml min-1 1.73 m-2). In the patients, fasting glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were determined using 125I-iothalamate and 131I-hippuran, respectively, during near-normoglycaemia. On a separate day, the levels of glucagon and GH were determined in the fasting basal state and after exercise. Multiple regression analysis disclosed that GFR was positively correlated with HbA1 (r2 = 0.18, p < 0.01), glucagon (r2 = 0.14, p < 0.03) as well as exercise-stimulated GH (r2 = 0.10, p < 0.05). ERPF was independently associated with HbA1 (r2 = 0.24, p < 0.005) and glucagon (r2 = 0.18, p < 0.01), whereas renal vascular resistance (RVR) was negatively correlated with stimulated GH (r2 = 0.18, p < 0.02). Kidney volume was positively correlated with HbA1 (r2 = 0.26, p < 0.001) and inversely with RVR (r2 = 0.16, p < 0.01), but not with glucagon or stimulated GH. The present study suggests that circulatory GH and glucagon play a contributory role in the renal haemodynamic changes in type 1 diabetes mellitus.

Adult↗

Long-term effects of linoleic-acid-enriched diet on albuminuria and lipid levels in type 1 (insulin-dependent) diabetic patients with elevated urinary albumin excretion.

We conducted a 2-year prospective randomised study to investigate the effects of a linoleic-acid-enriched diet on albuminuria and lipid levels in Type 1 (insulin-dependent) diabetic patients with elevated urinary albumin excretion (overnight urinary albumin excretion rate between 10 and 200 micrograms/min). Thirty-eight patients were randomly assigned to increase dietary polyunsaturated:saturated fatty acids ratio to 1.0 by replacement of saturated fat with linoleic-acid-rich products (n = 18, two dropouts, analysis was performed in n = 16) or to continue their usual diet (n = 20). The total fat and protein content of the diet was unaltered. Clinical characteristics, albuminuria, blood pressure, glomerular filtration rate, metabolic control and dietary composition were similar in the two groups at baseline. In the high linoleic acid diet group, linoleic intake rose from 7 +/- 4 to 11 +/- 2 energy % and polyunsaturated:saturated fatty acids ratio rose from 0.60 +/- 0.28 to 0.96 +/- 0.16 (p less than 0.001 compared to usual diet group). The median increase albuminuria was 58% (95% confidence interval, 13 to 109) during the first year (p less than 0.02) and 55% (95% confidence interval, 11 to 127) (p less than 0.01) during the second year. Glomerular filtration rate remained unaltered and filtration fraction tended to rise (p less than 0.05 compared to usual diet group). In the usual diet group, albuminuria did not significantly increased by 16% (95% confidence interval, -17 to 38) and glomerular filtration rate declined during the second year. Blood pressure tended to rise similarly in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Abnormal plasma noradrenaline response and exercise induced albuminuria in type 1 (insulin-dependent) diabetes mellitus.

Submaximal exercise provokes an abnormal elevation in albuminuria in type 1 (insulin-dependent) diabetes mellitus. Plasma catecholamines might be involved in this phenomenon by a renal vasoconstrictive effect. Twelve healthy subjects (Controls: albuminuria < 10 micrograms min-1), 13 normoalbuminuric type 1 diabetic patients (DNormo: albuminuria < 10 micrograms min-1) and 13 microalbuminuric type 1 diabetic patients (DMicro: albuminuria 10-200 micrograms min-1) performed a fixed bicycle workload (600 kpm for 20 min+urine collection 40 min post exercise). None of the patients suffered from autonomic neuropathy or hypertension. Fractional albumin clearance (FalbCl) rose in DNormo (p = 0.02) and DMicro (p = 0.01) but not in the Controls (p = 0.40). Basal plasma adrenaline and noradrenaline were not different in the three groups. The increments in noradrenaline were more pronounced in DNormo and DMicro than in Control (Controls < DNormo, p < 0.05; Controls < DMicro, p < 0.01). The changes in FalbCl were significantly correlated with the changes in noradrenaline (all subjects r = 0.65, p < 0.001). The increments in adrenaline were not different in the diabetic groups compared to the controls, and were not related to the changes in FalbCl. Multiple regression analysis showed that changes in plasma noradrenaline (p < 0.002) and in mean arterial pressure (p < 0.005) independently contributed to the changes in FalbCl (multiple r = 0.73). It is concluded that the exercise-induced plasma noradrenaline response is increased in normo- and microalbuminuric type-1 diabetic patients. Noradrenaline appears to contribute in the exercise-induced changes in renal protein handling, possibly by its effect on renal haemodynamics.

Adult↗

The activity of cholesteryl ester transfer protein is decreased in hypothyroidism: a possible contribution to alterations in high-density lipoproteins.

The activity of cholesteryl ester transfer protein is instrumental in the distribution of cholesteryl ester between lipoproteins in plasma. We measured the activity of cholesteryl ester transfer protein in plasma, designated cholesteryl ester transfer activity, as the rate of cholesteryl ester transfer between exogenous radiolabelled low-density and high-density lipoproteins. The effect of hypothyroidism on cholesteryl ester transfer activity was investigated in 13 athyreotic patients who were studied in the hypothyroid condition and in the euthyroid state, after they had received triiodothyronine supplementation for 33 to 67 days. During hypothyroidism plasma total cholesterol, very-low- plus low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, plasma triacylglycerol, apolipoprotein A1 and B were significantly higher than in the euthyroid state. Cholesteryl ester transfer activity was 15% lower during hypothyroidism (P less than 0.02), and an effect of treatment duration was observed. The changes in high-density lipoprotein total cholesterol (P less than 0.02), free cholesterol (P less than 0.001), triacylglycerol (P less than 0.05) and the free cholesterol/cholesteryl ester molar ratio in high-density lipoproteins (P less than 0.01) were inversely-related to the changes in cholesteryl ester transfer activity. We concluded that thyroid hormone is involved in the regulation of cholesteryl ester transfer protein activity, and that cholesteryl ester transfer protein activity may play a role in the alterations in high-density lipoprotein lipids observed in hypothyroidism.

Adult↗