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Biomedical subjects

I Mattiasson

Publications and source records attributed to I Mattiasson.

At least 37 records · Page 2Linked to original sources
PubMed1999

Heredity for hypertension influences intra-uterine growth and the relation between fetal growth and adult blood pressure.

OBJECTIVE: To study whether heredity for hypertension influences intra-uterine growth and the relationship between fetal growth and adult blood pressure. DESIGN: Five-year prospective follow-up study with retrospective collection of data on size at birth and gestational age from obstetric records. SETTING: Centre of preventive medicine in Malmo, Sweden. SUBJECTS: Thirty normotensive men with and 27 without heredity for hypertension were investigated in 1990, and the majority (n = 28 and n = 20, respectively) in 1995 also. MAIN OUTCOME MEASURES: Two measures of intra-uterine growth were compared between the groups and related to adult systolic blood pressure: the birth weight deviation from the expected birth weight based on ultrasonically derived intra-uterine growth curves, and the degree of thinness at birth (ponderal index = weight/length3). RESULTS: The birth weight deviation in men with heredity for hypertension differed significantly from that in men without such heredity (%) (-6.9+/-12.0 versus +7.3+/-18.4; P = 0.002). Ponderal index was somewhat lower in the men with than in those without heredity for hypertension, but the difference did not reach statistical significance (kg/m3) (25.9+/-2.6 versus 27.0+/-2.2; P = 0.08). In the group with heredity for hypertension, systolic blood pressure correlated inversely with ponderal index both in 1990 (r = -0.44; P = 0.01) and 1995 (r = -0.49; P = 0.009), and the 5-year increase in systolic blood pressure correlated inversely with the birth weight deviation (r = -0.38; P = 0.04). No such correlations were found in the group without heredity for hypertension. CONCLUSION: Our results suggest that genetic factors contributing to the development of hypertension may influence intra-uterine growth.

Adult↗
PubMed1999

Increasing plasma neopterin and persistent plasma endothelin during follow-up after acute cerebral ischemia.

Release of inflammatory mediators from leukocytes and endothelial release of vasoactive factors are both important in the pathogenesis of atherosclerosis. To evaluate the concentrations of a specific marker for macrophage activation, neopterin, and the potent endothelial derived vasoconstrictive peptide endothelin-1 (ET-1), during the acute and chronic stages of cerebral ischemia, plasma concentrations of neopterin and ET-1 were measured in 59 patients with acute cerebral infarction or transient ischemic attack (median age 73 years, range 43-93, 27 men) and after a 1-year follow-up in 57/59 (97%) of patients. Plasma neopterin was higher at follow-up (6.3 nmol/L [3.7-21.6] vs 5.6 nmol/L [3.5-17.2]; p < 0.05) than at the acute stage, whereas the plasma ET-1 concentration was unchanged. Plasma concentrations of both neopterin and ET-1 correlated directly with age both in the acute stage (r = 0.42 and r = 0.35, respectively; p < 0.01) and after follow-up (r = 0.34; p < 0.05 and r = 0.27; p = 0.05, respectively). In conclusion, plasma neopterin increased after acute cerebral ischemia, indicating chronic inflammatory activity and continuous macrophage activation in ischemic cerebrovascular diseases.

Acute Disease↗
PubMed1998

Insulin sensitivity, sodium-lithium countertransport and platelet free calcium concentrations in normotensive men with a family history of hypertension.

Peripheral glucose disposal (assessed with the euglycaemic-hyperinsulinaemic clamp technique), Na+-Li+ countertransport in erythrocytes and the cytosolic free Ca2+ concentration in platelets were determined in 36 men from families with essential hypertension in at least two close relatives and in 28 age- and weight-matched men from families without hypertension. All had diastolic blood pressure consistently below 90 mm Hg and a normal oral glucose tolerance test. The mean age of the study population as a whole was 37 years (range 24-46). Insulin sensitivity index values (glucose disposal/serum insulin concentration during the clamp) were lower in the familial hypertension group than in the control group, but the two groups did not differ in Na+-Li+-countertransport, or in the platelet cytosolic free Ca2+ concentration which was correlated to the waist: hip circumference ratio in both groups (r = 0.38 and r = 0.49, respectively). The present findings do not support the hypothesis that an increase in Na+-Li+ countertransport activity or the platelet cytosolic free Ca2+ concentration is a marker of insulin resistance in hypertension prone men.

Adult↗
PubMed1998

Muscle fibre composition and glycogen synthase activity in hypertension-prone men.

OBJECTIVES: To study muscle fibre characteristics and glycogen synthase activity in relation to peripheral glucose disposal in skeletal muscle in hypertension-prone men. DESIGN: The hyperinsuliemic euglycemic clamp method was used to calculate insulin sensitivity index (M/I). Muscle biopsies were performed for the analysis of slow-twitch (ST) and fast twitch (FT, low insulin sensitivity and low capillarisation compared to ST fibres) muscle fibres, capillarisation (number of capillaries per fibre) and diffusional index (mean area per fibre divided by capillarisation) of muscle fibres, capillary density (capillaries mm(-2) muscle fibre) and glycogen synthase activity. SUBJECTS: Thirty-two young, healthy, normotensive men with a family history of hypertension (REL) were compared to 2 5 age-matched men with no family history of hypertension (CON) and similar body mass index (BMI). RESULTS: REL had a lower M/I (P = 0.021), lower capillarisation (P = 0.04) and a tendency of a lower diffusional index of subgroup b of FT muscle fibres (P = 0.10) compared to CON. Glycogen synthase activity did not differ between the groups. CONCLUSIONS: Men with a family history of hypertension have less capillaries per FTb fibre and greater diffusion distance from the capillary to the muscle cell compared to controls, which may be a contributory factor to the lower insulin sensitivity in the former group. However, additional investigations are needed to study the causality in this association.

Adult↗
PubMed1998

Mutations and variants of the epithelial sodium channel gene in Liddle's syndrome and primary hypertension.

Liddle's syndrome is a rare monogenic form of hypertension caused by truncating or missense mutations in the C termini of the epithelial sodium channel beta- or gamma-subunits. These mutations delete or alter a conserved proline-rich amino acid sequence referred to as the PY-motif. We report here a Liddle's syndrome family with a betaArg564X mutation with a premature stop codon deleting the PY-motif of the beta-subunit. This family shows marked phenotypic variation in blood pressure, serum potassium levels, and age of onset of hypertension. Given the similarity with primary hypertension, changes in the C termini of the beta- or gamma-subunits may contribute to the development of primary hypertension or to hypertension associated with diabetic nephropathy. Accordingly, the coding sequences for the cytoplasmic C termini of the beta- and gamma-subunits were screened for mutations with the use of polymerase chain reaction, single-strand conformation polymorphism, and direct DNA sequencing in 105 subjects with primary hypertension and 70 subjects with diabetic nephropathy. One frequent polymorphism was identified, but its frequency did not differ among subjects with primary hypertension, subjects with diabetic nephropathy, or control subjects. Two of the 175 subjects with primary hypertension or diabetic nephropathy showed variants that were not present in 186 control subjects. None of the variants changed the PY-motif sequence. In conclusion, a betaArg564X mutation is the likely cause of Liddle's syndrome in this Swedish family, but it is unlikely that mutations in the beta- and gamma-subunit genes of the epithelial sodium channel play a significant role in the pathogenesis of primary hypertension or diabetic nephropathy.

Adult↗
PubMed1998

Endothelial derived vasoactive factors and leukocyte derived inflammatory mediators in subjects with asymptomatic atherosclerosis.

To clarify relationships between the (endothelial vasodilatory and vasoconstrictive function) and leukocyte inflammatory mediators in subjects with asymptomatic atherosclerosis, we measured (intraplatelet cyclic 3',5'-guanosine monophosphate [cGMP] and cyclic 3',5'-adenosine monophosphate [cAMP]), plasma endothelin (ET-1), and plasma neopterin in 197 subjects with asymptomatic atherosclerosis (median age 63 years, range 49-69 years). We measured neutrophil protease 4 (NP4), tumor necrosis factor (TNFmu), soluble tumor necrosis factor receptor-1 (sTNFR-1), and neutrophil gelatinase associated lipocalin (NGAL) in 152 of the 197 subjects. Intraplatelet cGMP correlated inversely with plasma ET-1 (r=-0.22; p=0.01), which confirms earlier in vitro data of the inhibitory effect of ET-1 on NO production and/or the cGMP mediated inhibitory effect of NO on ET-1 production. Plasma neopterin as well as NP4 correlated directly with intraplatelet cGMP (r=0.24; p<0.01 and r=0.33; p<0.001, respectively). Intraplatelet cAMP correlated directly with plasma TNFmu (r=0.17; p<0.05) and sTNFR-1 (r=0.20; p<0.05). The relationship between leukocyte derived inflammatory mediators and intraplatelet cyclic nucleotides suggest an antiaggregating effect of leukocytes upon platelets, which may constitute a negative feedback mechanism that inhibits platelet activation during the atherosclerotic inflammatory process.

Aged↗
PubMed1998

Out-patient treatment of acute deep vein thrombosis.

BACKGROUND: To assess whether uncomplicated deep vein thrombosis could be treated in an out-patient setting without increasing the frequency of complications, and to determine the proportion of patients with deep vein thrombosis, traditionally treated as in-patients at the Departments of Medicine, who are eligible for such treatment. METHODS: In a multicentre study, carried out at six hospitals of varying sizes and serving a population of about 600,000, consecutive patients over 18 years of age, with verified deep vein thrombosis, primarily presented as acute cases at the respective Departments of Medicine, were considered for treatment on an out-patient basis during a 1-year period. INTERVENTIONS: Those eligible for out-patient treatment were put on low molecular weight heparin and oral anticoagulants, and scheduled for daily attendance at the out-patient clinic of the respective Dept. of Medicine. Details of any complication were recorded according to a standard check-list. The patients underwent a full checkup at three-month follow-up. MAIN OUTCOME MEASURES: Any bleeding event or pulmonary embolism. Progress of thrombosis. RESULTS: Of 523 patients considered for out-patient treatment, 126 (24%) were excluded according to the defined exclusion criteria, 197 (38%) were treated entirely on an out-patient basis, and another 43 (8%) were initially treated in hospital (median two days) before being transferred to the out-patient setting. Three patients had to be hospitalized for suspected complications, but none of these turned out to be serious. No serious bleeding event or thromboembolic complication was registered. CONCLUSIONS: Uncomplicated acute deep vein thrombosis could be safely treated on an out-patients basis. At least 50% of the patients with this diagnosis, former treated as in-patients at the Depts. of Medicine, are eligible for such treatment.

Acute Disease↗
PubMed1997

The factor VR506Q mutation causing APC resistance is highly prevalent amongst unselected outpatients with clinically suspected deep venous thrombosis.

OBJECTIVE: Resistance to activated protein C (APC resistance), caused by a single point mutation in the factor V gene (FV:R506Q), is a major risk factor for venous thrombosis. As the significance of this mutation among unselected outpatients with deep-vein thrombosis (DVT) is not established, we have studied its prevalence among consecutive outpatients attending the emergency room due to a clinically suspected DVT. DESIGN, SETTING AND SUBJECTS: The FV:R506Q mutation was determined in 223 consecutive Swedish outpatients with clinically suspected DVT, and in 288 healthy controls. Using phlebography, the patients were classified as DVT-positive or DVT-negative. MAIN OUTCOME MEASURE: The prevalence of FV:R506Q mutation. RESULTS: The prevalence of the FV:R506Q mutation was 28% (28/99) in the DVT-positive subgroup (relative risk: 3.1; 95% CI: 1.7-5.5), and 23% (28/124) in the DVT negative subgroup (relative risk: 2.0; 95% CI: 1.1-3.6), as compared to 11% (32/288) in the control group. In the DVT-positive subgroup, the FV:R506Q mutation was most common among younger patients with primary thrombosis (47%) and least common among older patients with secondary thrombosis (19%). The high prevalence of FV:R506Q mutation among DVT-negative patients was associated with a high frequency of previous venous thrombosis. Thus, 46% (13/28) of the DVT-negative FV:R506Q carriers had a history of thrombosis, compared with only 22% (21/96) of the DVT-negative patients lacking the mutation (P = 0.01). CONCLUSION: To sum up, the FV:R506Q mutation is present in more than a quarter of Swedish DVT-positive outpatients with clinically suspected DVT, indicating that APC-resistance is a major thrombotic risk factor contributing to the high incidence of venous thrombosis in Sweden.

Adult↗
PubMed1996

Cardiovascular risk groups and mortality in an urban swedish male population: the Malmö Preventive Project.

OBJECTIVES: To describe the size, overlap and mortality of four cardiovascular risk groups, in order to give a scientific background for the prevention of cardiovascular disease in a representative urban population. SETTING: Section of Preventive Medicine, Department of Medicine, Malmö University Hospital, Malmö, Sweden. SUBJECTS: Between 1974 and 1984 22444 men born between 1949 and 1921, constituting 75% of the total male population in these age groups, took part in a comprehensive screening examination aimed at detecting risk factors for cardiovascular disease. INTERVENTIONS: Those at high-risk of developing cardiovascular disease were referred to their general practitioner or to special clinics for hypertension, hyperlipidaemia and diabetes. The follow-up, which lasted until the end of 1991, averaged 12.2 years. MAIN OUTCOME MEASURES: Total death (n = 1450) and death from ischaemic heart disease (IHD) (n = 471). RESULTS: Hypertension was found in 13%, hypercholesterolaemia in 19% and diabetes mellitus in 2.6% of the subjects; 49% of the subjects smoked. Multiple risk factors were found in over 17% of the total cohort. Despite the intervention, all-cause mortality during follow-up was increased three-fold in smokers and in men with hypercholesterolaemia, four-fold in hypertensive men and five-fold in men with diabetes, compared to men with no risk factors. The vast majority of deaths (81%) occurred in men who smoked, had hypertension or had high serum cholesterol. Ischaemic heart disease (IHD) was increased five-fold in smokers, seven-fold in men with hypercholesterolaemia, nine-fold in hypertensive men and 12-fold in men with diabetes. Again, the vast majority of IHD deaths (86%) occurred in the first three categories. Combinations of risk factors substantially increased total mortality as well as IHD mortality. CONCLUSIONS: The large proportion (64%) of the population with risk factors for cardiovascular disease and the substantially (5-12-fold) increased IHD mortality in those risk groups, calls for actions aimed at preventing premature IHD deaths. Such action should include measures directed towards the whole population and comprehensive treatment programmes for high-risk individuals, including intervention to stop smoking. The substantial overlap between risk factors calls for one high-risk clinic caring for all risk groups.

Adult↗
PubMed1996

Coagulation and fibrinolytic factors in normotensive hypertension-prone men.

OBJECTIVE: To evaluate whether a family history of hypertension is associated with disturbances in the coagulation and fibrinolytic systems. SUBJECTS: Thirty-five normotensive men with a family history of hypertension (relatives) and 27 age- and body mass index-matched controls with a family history (controls). METHODS: Insulin sensitivity was determined with a euglycaemic hyperinsulinaemic clamp technique. Maximal oxygen uptake was estimated from a submaximal work test. Blood samples were analysed for several coagulation and fibrinolytic factors. RESULTS: Relatives had higher plasma levels of plasminogen activator inhibitor-1. Levels of plasma factor VII, prothrombin fragments 1 and 2, fibrinogen and von Willebrand factor antigen did not differ significantly between the groups. However, antithrombin III, protein C and protein S levels were higher in the relatives than in the controls. Coagulation and fibrinolytic factors correlated to waist circumference, insulin sensitivity, maximal oxygen uptake and serum triglycerides level. CONCLUSIONS: Normotensive men with a family history of hypertension have an inhibited fibrinolysis, but also higher levels of several anticoagulant factors. The clinical application of these findings for the future development of cardiovascular disease warrants additional studies.

Adult↗
PubMed1996

Intraplatelet cyclic 3'-5' guanosine monophosphate is related to serum cholesterol.

Nitric oxide (NO) exerts its vasodilator and antiaggregatory effects through activation of soluble guanylate cyclase and the consequent increase in the concentration of cGMP in target cells. We conducted this study in order to evaluate relationships between intraplatelet cGMP levels and risk factors for atherosclerosis in middle aged subjects. Intraplatelet cGMP was determined by radioimmunoassay and related to age, BMI, blood pressure, antihypertensive treatment, total, LDL and HDL cholesterol, triglycerides, blood glucose, HbA1c, smoking habit and intimal thickness of the common carotid artery in 265 subjects participating in a health survey (age 59 +/- 6 years, range 48-68 years, 121 females, 144 males). Intraplatelet cGMP concentration was inversely correlated with total serum cholesterol (r = -0.18; p < 0.01) and HDL cholesterol (r = -0.14, p < 0.05) as well as with platelet count (r = -0.29; p < 0.001). When platelet count was adjusted for, only the correlation between total serum cholesterol and cGMP remained significant. No significant correlations could be demonstrated between intraplatelet cGMP levels and measurable parameters of atherosclerosis. Lower levels of the vasodilating and antiaggregating mediator cGMP in platelets are related to higher levels of serum total cholesterol. These results favour the hypothesis of a relationship between lipid levels and NO associated vasodilator and antiaggregating function in atherosclerosis.

Age Factors↗
PubMed1996

Low testosterone and insulin resistance in hypertension-prone men.

The aim of the study was to elucidate the relationship between peripheral insulin sensitivity and testosterone and sex hormone binding globulin (SHBG) in the development of hypertension. An euglycaemic hyperinsulinaemic clamp was performed to determine insulin sensitivity and sex steroid hormones and SHBG were analysed in 35 normotensive men with a family history of hypertension (relatives) and 27 age and body mass index matched controls (controls). Relatives had lower concentrations of serum total testosterone and SHBG, and lower insulin sensitivity compared to controls. Free testosterone concentrations were the same in both groups. Relatives had lower maximal oxygen uptake compared to controls. Total testosterone and SHBG were correlated to basal insulin concentration and insulin sensitivity in relatives, but not in controls. In stepwise regression analysis, total testosterone explained 37% and walst circumference 6% of the variation of insulin sensitivity in relatives, and walst circumference explained 29% in controls. When substituting testosterone with SHBG in this model, SHBG explained 48% of the variation in insulin sensitivity in relatives. The finding of a closer relationship between insulin sensitivity and SHBG than between insulin sensitivity and total testosterone suggests that the SHBG level is primarily influenced by insulin sensitivity in the relatives.

Estradiol↗
PubMed1995

Insulin and forearm vasodilation in hypertension-prone men.

Insulin-stimulated peripheral glucose uptake and insulin-mediated forearm vasodilation were investigated in 38 normotensive men with a family history of hypertension (relatives) compared with 27 age- and body mass index-matched normotensive men with no family history of hypertension (control subjects). The euglycemic hyperinsulinemic clamp technique was used to measure peripheral glucose uptake (insulin sensitivity index) and the metabolic clearance rate of insulin. Intra-arterial blood pressure and forearm blood flow were determined simultaneously, and forearm vascular resistance was calculated. The insulin sensitivity index was lower in relatives than in control subjects. The metabolic clearance rate of insulin was reduced and did not correlate to glucose disposal in the relatives as opposed to the control subjects. Forearm blood flow increased and forearm vascular resistance decreased to a similar extent in the two groups during the clamp. The vasodilator response was positively correlated to glucose disposal only in the relatives. In conclusion, impaired insulin-stimulated peripheral glucose uptake in normotensive sons from hypertensive families was accompanied by retained insulin-mediated forearm vasodilation. Thus, skeletal muscle blood flow supply does not seem to be the major determinant for glucose disposal. On the other hand, the positive correlation between glucose disposal and decrease in forearm vascular resistance in the relatives suggests that insulin-mediated vasodilation may be a limiting factor for peripheral glucose uptake in insulin-resistant individuals.

Disease Susceptibility↗
PubMed1995

Blood pressure and myocardial perfusion in hypertensive patients with and without left ventricular hypertrophy.

To evaluate the effect of acute blood pressure (BP) changes on the myocardial perfusion in hypertensives, 10 patients with and 10 patients without left ventricular hypertrophy (LVH) were examined with 99TCm-Sestamibi scintigraphy at rest and after acute pharmacological BP reduction using nifedipine and captopril. Signs of LV ischaemia was quantified as the size of the hypoperfused area defined as isotope uptake below 70% of maximum LV uptake, and LVH was defined as ventricular mass (LVM) > 125 g/m2 BSA by use of echocardiography. Not significant relations between BP and size of the hypoperfused area was found at rest. During BP reduction patients with LVH had negative correlations (r = -0.58) between the size of the hypoperfused area and the systolic blood pressure (SBP) and the diastolic blood pressure (DBP) (r = -0.49) while patients without LVH showed positive correlations (SBP r = 0.60, DBP r = 0.48). The differences in correlation coefficients were significant (P < 0.01) for both. Thus, in hypertensives with LVH, ischaemia may develop at low BP providing a possible mechanism for the observed increased risk of cardiovascular events in some hypertensive patients with low achieved BP during follow-up. Until treatment goals are defined on scientific grounds, BP should not be decreased below 90 mm Hg in subjects with LVH.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1994

Insulin and renal sodium retention in hypertension-prone men.

Insulin-stimulated peripheral glucose uptake and insulin-induced renal tubular sodium reabsorption were investigated in normotensive men with a family history of hypertension (relatives, n = 35) compared with age- and body mass index-matched normotensive men with no family history of hypertension (controls, n = 23). The effect of insulin on the renin-aldosterone system was also studied. The euglycemic hyperinsulinemic clamp technique was used to measure peripheral glucose uptake (insulin sensitivity index). Renal clearance of 51Cr-labeled EDTA, sodium, and lithium was used to calculate fractional excretion of sodium and fractional proximal and distal tubular reabsorption of sodium before and during insulin infusion. The insulin sensitivity index was lower in relatives than in controls. Fractional excretion of sodium was reduced, and fractional proximal and distal tubular reabsorption of sodium were increased to the same extent in both groups during insulin infusion. Fractional distal tubular reabsorption of sodium was positively correlated to the reduction of serum potassium in all individuals. Plasma renin activity increased to the same extent in both groups, whereas plasma aldosterone was reduced only in controls. In conclusion, the impaired insulin-stimulated glucose uptake in peripheral tissues in normotensive sons of hypertensive families was accompanied by retained insulin-induced tubular sodium reabsorption. The lack of suppression of aldosterone secretion in these individuals may enhance sodium retention.

Absorption↗
PubMed1994

Metabolic control in insulin-dependent diabetes mellitus, as reflected in the in vitro effects of platelets on endothelial cell proliferation and prostacyclin production.

We tested the hypothesis that the degree of metabolic control in diabetes mellitus may be a determinant of the ability of platelets to stimulate proliferation of endothelial cells (ECs) and smooth muscle cells (SMCs). Platelets were obtained from 24 patients (two groups of 12 patients each) with insulin-dependent diabetes mellitus (IDDM) and increased blood glucose concentrations (HbA1c > 10% Hb), duration of disease 2-45 years, on no other medication than insulin at the time of blood sampling or during the preceding 6 months, and with no signs of coronary artery disease, nephropathy, hypertension or retinopathy. The patients served as their own controls, platelets being obtained from them again 2-4 months later when their mean glucose values were lower (HbA1c < 6.5% Hb). EC proliferation was significantly reduced after exposure to platelets obtained from the patients when their metabolic control had improved, whereas no significant differences were seen in either SMC proliferation or prostacyclin production. There was no correlation between changes in insulin dosage and either cell proliferation or prostacyclin production, or between changes in lipid values and cell proliferative capacity. It is concluded that, EC proliferation will be greater, owing to the platelet effects found in vitro, when metabolic control in diabetics is poor than when it is good, which may be of importance regarding the repair of endothelial lesions.

Adult↗
PubMed1994

Insulin resistance is coupled to low physical fitness in normotensive men with a family history of hypertension.

OBJECTIVE: To investigate insulin sensitivity and the influence of level of physical fitness in men with a family history of hypertension and in control subjects. DESIGN: Insulin sensitivity was determined and physical fitness estimated in 39 normotensive, glucose-tolerant men with a family history of hypertension (Relatives group) and in 29 age- and body mass index-matched normotensive men with no such family history (Controls group). METHODS: The euglycaemic hyperinsulinaemic clamp technique (steady-state insulin concentration approximately 100 mU/l) was used to determine insulin sensitivity. Physical fitness, measured as maximal oxygen uptake, was estimated from the heart rate response to a submaximal exercise test. RESULTS: Insulin sensitivity index and estimated maximal oxygen uptake were lower in the Relatives than in the Controls. There was a positive correlation between insulin sensitivity and maximal oxygen uptake in both groups. In the Controls there was a negative correlation between insulin sensitivity and waist:hip ratio, but this relationship was not found in the Relatives. CONCLUSIONS: The present findings indicate that reduction of insulin sensitivity precedes the development of high blood pressure and may be coupled to low physical fitness. As abdominal fat distribution seems not to be related to insulin sensitivity in subjects with a family history of hypertension, changes in muscle fibre composition or muscle glucose metabolism, or both, might explain the lower insulin sensitivity and physical fitness in the Relatives.

Adult↗