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Biomedical subjects

J Johansson

Publications and source records attributed to J Johansson.

At least 145 records · Page 8Linked to original sources
PubMed1995

Localization of autosomal dominant cerebellar ataxia associated with retinal degeneration and anticipation to chromosome 3p12-p21.1.

We present linkage analysis on a large Swedish five-generation family of 15 affected individuals with autosomal dominant cerebellar ataxia (ADCA) associated with retinal degeneration and anticipation. Common clinical signs in this family include ataxia, dysarthria and severely impaired vision with the phenotype ADCA type II. Different subtypes of ADCA have proven difficult to classify clinically due to extensive phenotypic variability within and between families. Genetic analysis of a number of ADCA type I families shows that heterogeneity exists also genetically. During the last few years several types of ADCA type I have been localized and to date six genetically distinct forms have been identified including SCA1 (6p), SCA2 (12q), SCA3 and Machado-Joseph disease (MJD) (14q), SCA4 (16q), and finally SCA5 (11). We performed a genome-wide search of the Swedish ADCA type II family using a total of 270 microsatellite markers. Positive lod scores were obtained with a number of microsatellite markers located on chromosome 3p12-p21.1. Three markers gave lod scores over 3 with a maximum lod score of 4.53 achieved with the marker D3S1600. The ADCA type II gene could be restricted to a region of 32 cM by the markers D3S1547 and D3S1274.

Cerebellar Ataxia↗
PubMed1995

Postoperative pulmonary vascular supply in congenital heart disease evaluated with MR imaging at 0.3 T.

The aim of this study was to investigate the usefulness of static spin-echo MR imaging at low field strength in evaluating postoperative pulmonary arterial supply. Twenty-seven patients operated on for complex congenital heart disease underwent cardiac MR imaging: 27 stenoses in 20 patients and 4 aneurysms were present in the material. Five of the overlooked stenoses were located in the ventricular outflow tract or in the valvular region. All four aneurysms were well depicted. The final diagnosis were based on two-dimensional echocardiography, Doppler and invasive studies. MR correctly evaluated the pulmonary arterial supply in 21 patients. In two cases the evaluation was incomplete and in the remaining four patients MR failed to show the stenoses. MR imaging at 0.3 T is an effective non-invasive tool for postoperative evaluation of pulmonary arteries.

Adolescent↗
PubMed1995

Predilection of atherosclerosis for the inner curvature in the femoral artery. A digitized angiography study.

The degree of atherosclerosis in the inner and outer curvature of the femoral artery was studied by using digitized angiography and edge-roughness calculations in 301 hyperlipidemic patients. When the two edges of the vessel were compared no significant difference was seen, but when the local curvature was taken into account, inner curves were found to be more atherosclerotic than outer curves, and both inner and outer curves were more affected than straight segments. The same pattern was encountered in subpopulations defined by clinical or blood lipid criteria. The suggested explanation is that flow disturbances such as low shear rates or separated flow, which tend to arise along the inner curvature, promote the development of atherosclerosis.

Adult↗
PubMed1995

Lowering of HDL2b by probucol partly explains the failure of the drug to affect femoral atherosclerosis in subjects with hypercholesterolemia. A Probucol Quantitative Regression Swedish Trial (PQRST) Report.

The aim of the Probucol Quantitative Regression Swedish Trial (PQRST) (n = 303) was to investigate whether probucol (0.5 g BID) added to diet and cholestyramine (8 g BID) could retard progression or induce regression of femoral atherosclerosis in hypercholesterolemic (> 6.86 mmol/L) subjects. Probucol did not induce regression over the 3-year trial period as estimated by change in lumen volume on quantitative arteriography of a 20-cm segment of the femoral artery. In this report we studied in a representative subgroup (n = 72) whether the reduction in HDL concentrations induced by probucol could explain the failure of the drug to be effective. We analyzed the effects of treatment on HDL particle size subclasses. Probucol lowered the relative level of HDL2b, comprising the largest HDL particles, by 53% and the protein concentration of HDL2b by 67%. The protein reduction in HDL was mainly confined to the apolipoprotein A-I moiety. The change in lumen volume correlated significantly with change in HDL, ie, HDL cholesterol (r = .34, P < .01), HDL2 cholesterol (r = .37, P < .01), HDL2b protein (r = .44, P < .001), and the relative HDL2b value (r = .51, P < .001). The corresponding values for relative HDL2b, distribution calculated on the active (n = 35) and placebo (n = 37) groups separately were also significant (r = .39 and .32, respectively; both P < .05). The correlation between drug-induced change in the relative HDL2b concentration and change in atherosclerosis was independent of the alteration in triglyceride concentration and could not be explained by treatment interaction.(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoprotein A-I↗
PubMed1995

Probucol treatment decreases serum concentrations of diet-derived antioxidants.

The effect of probucol, which is both a cholesterol-lowering drug and an antioxidant, on the serum concentrations of diet-derived antioxidants vitamin E, beta-carotene, lycopene, and vitamin A was studied in 303 hypercholesterolemic subjects. In a 3-year, double-blind, randomized trial we investigated to determine whether combined treatment with diet, cholestyramine, and probucol could reduce the progression of femoral atherosclerosis. Serum and lipoprotein antioxidant levels were measured by reverse-phase high-performance liquid chromatography. Cholestyramine significantly lowered serum concentrations of vitamin E by 7%, beta-carotene by 40%, and lycopene by 30% (all P < .001) due to impairment of gastrointestinal absorption and to serum cholesterol lowering. Probucol reduced serum vitamin E by 14% (P < .001) secondary to cholesterol and triglyceride lowering. The carotenoids were reduced by probucol by 30% to 40% (P < .001) most probably due to reductions in lipoprotein particle size and to competition with these substances for incorporation into VLDL during its assembly in the liver. This study shows that the use of a lipid-soluble antioxidant and cholesterol-lowering drug may have unfavorable effects on blood levels of diet-derived antioxidants.

Antioxidants↗
PubMed1994

The effect of probucol on femoral atherosclerosis: the Probucol Quantitative Regression Swedish Trial (PQRST).

The Probucol Quantitative Regression Swedish Trial tested whether treatment of hypercholesterolemic persons with probucol for 3 years affected femoral atherosclerosis. The primary end point was the change in atheroma volume estimated as change in lumen volume of the femoral artery assessed by quantitative arteriography. Three hundred three patients with visible atherosclerosis were randomized to probucol 0.5 g, twice daily, or to placebo. All patients were given diet and cholestyramine, 8 to 16 g/day. Twenty-nine patients were excluded because of inadequate primary end point measurements. The mean age of the remaining 274 subjects (158 were men) was 55 years. Seventeen percent had intermittent claudication and 24% had angina pectoris. After 3 years, the probucol-treated patients had 17% lower serum cholesterol, 12% lower low-density lipoprotein cholesterol, 24% lower total high-density lipoprotein cholesterol, and 34% lower high-density lipoprotein2 cholesterol levels than control subjects. All lipoprotein differences between the treatment groups remained highly significant during the trial. There was no statistically significant change in lumen volume between the probucol and the control group. Furthermore, there was no difference between the treatment groups with regard to change in arterial edge roughness or amount of aorto-femoral atherosclerosis; neither were there any differences between the treatment groups with regard to change in ST-segment depressions on exercise tests or ankle/arm blood pressure (secondary end points). In the control group, lumen volume increased (p < 0.001) and roughness of the femoral artery decreased (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Arteriosclerosis↗
PubMed1994

Influence of lipoprotein lipids, dietary fat and smoking on macrophage degradation of native and oxidized low density lipoprotein.

Relatively little is known about the biological mechanisms by which lipoproteins promote atherogenesis. It has, however, been shown that structural modification of low density lipoprotein (LDL), such as by oxidation, results in their uptake and degradation by intimal macrophages and consequently leads to formation of lipid-rich atherosclerotic lesions. The aim of the present investigation was to study the influence of dietary intake of fat, lipoprotein lipid composition, smoking and gender on macrophage degradation of LDL before and after oxidation. The study group consisted of 48 males and 56 females with hyperlipidemia taking part in the open prerandomization phase of the Probucol Quantitative Regression Swedish Trial (PQRST). Analysis including lipoprotein determinations, dietary and smoking habit interviews, LDL degradation by macrophages, LDL receptor binding and LDL thiobarbituric acid reactive substance (TBARS) levels before and after copper ion-induced oxidation was done during the pre-andomization phase of the study. Increased plasma and very low density lipoprotein (VLDL) triglyceride levels were associated with an increased macrophage degradation of native LDL, whereas no such association was found after oxidation of LDL. The dietary intake of polyunsaturated fatty acids (PUFA) was also inversely related to the degradation of native LDL by macrophages, but increased the rate at which oxidized LDL was degraded. Smoking and gender did not influence the rate of macrophage degradation of native or oxidized LDL. It is concluded that hypertriglyceridemia is associated with an increased macrophage degradation of LDL. This may represent a mechanism by which hypertriglyceridemia promotes atherosclerosis.

Adult↗
PubMed1994

Secondary structure and membrane interaction of PR-39, a Pro+Arg-rich antibacterial peptide.

PR-39 is a 4719-Da peptide isolated from pig intestine and belonging to the recently discovered family of Pro+Arg-rich antibacterial peptides. PR-39 does not lyse Escherichia coli, instead the lethal action is probably linked to the termination of DNA and protein synthesis [Boman, H. G., Agerberth, B. & Boman, A. (1993) Infect. Immun. 61, 2978-2984]. Circular dichroism and Fourier-transform infrared spectroscopy have been used to investigate the secondary structure of PR-39 in the absence or presence of lipids. According to the circular dichroic data, this structure is not altered upon incubation of PR-39 with negatively charged vesicles, although the infrared spectra suggest that the hydrogen bond pattern is modified upon the peptide-lipid interaction. This is detected by a shift in the maximum wavelength of absorption of PR-39 from 1636 cm-1 in the absence of lipids to 1645 cm-1 in the presence of lipids. We have further addressed the question of the possible mechanism of interaction of PR-39 with model membranes (liposomes and planar lipid bilayers) whose lipid compositions mimick that of the E. coli inner membrane. PR-39 induced a calcein release from large unilamellar vesicles, which is dependent upon the peptide concentration and upon the presence of negatively charged lipid (glycerophosphoglycerol) in the membrane. The binding study of PR-39 to dioleoylglycerophosphoglycerol vesicles suggests that nearly 100% of the added peptide is membrane-bound. Addition of PR-39 to a planar lipid bilayer induced a linear increase in the current but no channel formation was observed since no discrete steps of conductance occurred.

Animals↗
PubMed1994

The NMR structure of the pulmonary surfactant-associated polypeptide SP-C in an apolar solvent contains a valyl-rich alpha-helix.

The nuclear magnetic resonance (NMR) structure of the pulmonary surfactant-associated lipoplypeptide C (SP-C) was determined in a mixed solvent of C2H3Cl/C2H3OH/ 1 M HCl 32:64:5 (v/v). Sequence-specific 1H NMR assignments and the collection of conformational constraints were achieved with two-dimensional 1H NMR, and the structure was calculated with the distance geometry program DIANA. The root mean square deviations for the well-defined polypeptide segment of residues 9-34 calculated for the 20 best energy-minimized DIANA conformers relative to their mean are 0.5 and 1.3 A for the polypeptide backbone atoms N, C alpha, and C', and for all heavy atoms, respectively. The 35-residue polypeptide chain of SP-C forms an alpha-helix between positions 9 and 34, which includes two segments of seven and four consecutive valyls that are separated by a single leucyl residue. The N-terminal hexapeptide segment, which includes two palmitoylcysteinyls, is flexibly disordered. The length of the alpha-helix is about 37 A, and the helical segment of residues 13-28, which contains exclusively aliphatic residues with branched side chains, is 23-A long and about 10 A in diameter. The alpha-helix is outstandingly regular, with virtually identical chi 1 angles for all valyl residues. The observation of a helical structure of SP-C was rather unexpected, considering that Val is generally underrepresented in alpha-helices, and it provides intriguing novel insights into the structural basis of SP-C functions as well as into general structural aspects of protein-lipid interactions in biological membranes.

Amides↗
PubMed1994

Laser-induced fluorescence in malignant and normal tissue in mice injected with two different carotenoporphyrins.

Laser-induced fluorescence (LIF) was used to characterise the localisation of an intravenously administered trimethylated carotenoporphyrin [CP(Me)3] and a trimethoxylated carotenoporphyrin [CP(OMe)3] in an intramuscularly transplanted malignant tumour (MS-2 fibrosarcoma) and healthy muscle in female Balb/c mice, 3, 24, 48 and 96 h post injection. The fluorescence was induced with a dye laser pumped by a nitrogen laser, emitting light at 425 nm. The fluorescence spectra were recorded in the region 455-760 nm using a polychromator equipped with an image-intensified CCD camera. The tumour/peritumoral muscle ratio was about 5:1 for CP(Me)3 and about 6:1 for CP(OMe)3 in terms of the background-free fluorescence intensity, which peaked at about 655 nm. By including the endogenous tissue fluorescence, the contrast was further enhanced by a factor of approximately 2.

Animals↗
PubMed1994

Safety, immunogenicity and an open, retrospective study of efficacy of a monocomponent pertussis toxoid vaccine in infants.

One hundred forty-five infants were vaccinated with 25 micrograms of pertussis toxoid (NICHD-Ptxd) at 3, 5 and 7 or at 3, 5 and 12 months of age. One month after the third vaccination all had high serum IgG and neutralizing antibodies (antitoxin) against pertussis toxin. Vaccination at 3, 5 and 12 months resulted in higher antibody titers than vaccination at 3, 5 and 7 months. Sera obtained from 109 children at 3 years of age showed a decline of antibodies, but all had detectable antibodies. Adverse reactions were confined to local redness and swelling, which exceeded 2 cm after 17% of all injections. When the children were 3 years old, a comparison was made of the incidence of clinical pertussis in 142 of the 145 vaccinated children and in 284 age-matched controls living in the same areas. Information on symptoms of pertussis was obtained from the parents during telephone interviews. None of the vaccinated children had clinical pertussis, defined as a 6-week course of paroxysmal cough with whooping attacks or vomiting, whereas 57 controls (20%) had experienced these symptoms. Sixteen vaccinated children were exposed to pertussis in the household. Two of them had laboratory-verified Bordetella pertussis infections with cough of 2 and 4 weeks, respectively, without whooping attacks or vomiting, whereas 14 did not develop a cough. The study shows that NICHD-Ptxd is immunogenic in infants and that it most likely confers a high degree of protection against pertussis.

Antibodies, Bacterial↗
PubMed1994

Photodynamic therapy of non-melanoma malignant tumours of the skin using topical delta-amino levulinic acid sensitization and laser irradiation.

Eighty basal cell carcinomas (BCCs) in 21 patients, 10 lesions of Bowen's disease in three patients, and four lesions of cutaneous T-cell lymphoma in two patients, were treated with photodynamic laser therapy (PDT), using topical application of the haem precursor delta-amino levulinic acid (ALA). The diagnoses were confirmed histologically prior to treatment. Fifty-five of the BCCs were superficial lesions, and 25 were nodular. Of the 80 BCCs, 39 (49%) were located on the trunk, 36 (45%) on the head and neck region, four (15%) on the leg and one on the arm. The two principal locations of the 10 Bowen's disease lesions were the leg (50%) and the trunk (40%). The T-cell lymphoma lesions were located on the shoulder and on the arm. A water-in-oil based cream containing 20% ALA was applied to the lesions, with a margin of about 10-20 mm beyond the visible tumour border, 4-6 h before the laser procedure. During this period of time the highly fluorescent and photodynamically active substance protoporphyrin IX (Pp IX) is synthesized via the haem cycle. Laser-induced fluorescence (LIF) was used for real-time monitoring of the Pp IX distribution in the tumour and in the normal surrounding skin, before and after treatment in all patients. Before laser treatment the Pp IX distribution demonstrated by LIF showed a demarcation between tumour and normal skin of about 15:1 for BCC and Bowen's disease, and 5:1 for T-cell lymphomas.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Topical↗
PubMed1994

The relation of coronary and peripheral arterial disease to the severity of femoral atherosclerosis in hypercholesterolaemia.

OBJECTIVES: The extent of atherosclerosis in the superficial femoral artery and the severity of arterial disease in the aorto-iliac and femoro-popliteal arterial districts were related to clinical diagnosis of coronary and peripheral atherosclerosis in hypercholesterolaemic patients. DESIGN: The study constitutes baseline cross-sectional data of a randomized double-blind clinical trial on Probucol, using both computer based and visual estimations of angiographies as endpoints. SUBJECTS: Two hundred and ninety men and women (mean age 54 years) with hypercholesterolaemia. MAIN OUTCOME MEASURES: Atherosclerosis was estimated with arteriographies. Lumen volume and edge roughness (vessel inner wall irregularity) of a 20 cm segment of the femoral artery were estimated by computer. A visual atherosclerosis score of the abdominal aorta to the popliteal arteries was made on both sides. RESULTS: Patients with peripheral arterial disease had significantly more advanced disease according to all three angiographic variables than those without symptoms of peripheral vascular disease. Both men and women with coronary artery disease had significantly lower femoral lumen volume and higher roughness values than patients without. Men with previous myocardial infarction had significantly higher mean visual scores of atherosclerosis than those without, while lumen volume and roughness did not differ in either sex. CONCLUSIONS: Femoral atherosclerosis is an expression of a generalized disease, associated with clinical symptoms of coronary artery disease. Femoral atherosclerosis is often accompanied by atherosclerosis also in the coronary arteries.

Adult↗
PubMed1994

Associations of genotypes at the apolipoprotein AI-CIII-AIV, apolipoprotein B and lipoprotein lipase gene loci with coronary atherosclerosis and high density lipoprotein subclasses.

Association studies were carried out in a sample of 86 patients from Sweden who had survived a myocardial infarction (MI) at a young age and 93 age-matched healthy individuals, to compare the impact of polymorphisms at the apolipoprotein (apo) AI-CIII-AIV gene cluster on among-individual differences in plasma lipid and lipoprotein traits, the five high density lipoprotein (HDL) subclasses (2b to 3c), lipoprotein lipase (LPL) activity and presence and progression of atherosclerosis. Individuals were genotyped for four polymorphisms; 5'apoAI (G/A-75), 3'apoAI (PstI; P +/-), apoCIII (C/T1100) and apoCIII (PvuII; V +/-), using PCR-based techniques. Allele frequencies were similar in healthy individuals and patients (frequencies of alleles in combined population: 5'apoAI-A-75 = 0.14, 3'apoAI-P- = 0.05, apoCIII-T1100 = 0.27 and apoCIII-V- = 0.18). In the healthy individuals, levels of low density lipoprotein (LDL) triglycerides were significantly associated with genotypes of the apoCIII-PvuII polymorphism (p = 0.02), but no other associations were found between lipids or HDL subclasses and single polymorphisms in the apoAI-CIII-AIV gene cluster. Levels of triglycerides and very low density lipoprotein (VLDL) triglycerides were significantly higher in the presence of the haplotype defined by the presence of apoCIII-T1100 and common alleles of the other three polymorphisms, explaining 5.8% and 7.8% (p = 0.03 and 0.01), respectively, of sample variance. In the patients, no associations were found between lipids or HDL subclasses and variation at the apoAI-CIII-AIV gene cluster. Associations were also examined between levels of HDL subclasses and variation at the apoE (common isoforms), apoB (signal peptide and XbaI polymorphisms) and lipoprotein lipase (PvuII, HindIII and Serine447/Stop polymorphisms) gene loci. In the patient group only, levels of protein in HDL2b, HDL2a and HDL3b subclasses were significantly associated with genotypes of the LPL-HindIII polymorphism (22.1, 19.3 and 11.4%, respectively, of sample variance; p < 0.05). Finally, associations were examined between genotypes at the apoAI-CIII-AIV gene cluster and the extent of coronary atherosclerosis. Global severity of atherosclerosis at the first angiography was weakly associated with genotypes of the apoCIII-C/T1100 polymorphism, presence of the T1100 allele being associated with 53% lower median score (1.6 vs 0.75; p = 0.09).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1994

The proteins of the surfactant system.

The structural and functional integrity of pulmonary surfactant depends on several specific proteins. Two of these, SP-A and SP-D, are large and water-soluble, while SP-B and SP-C are small and very hydrophobic. SP-A is an 18-mer of 26 kDa polypeptide chains and contains N-linked oligosaccharides. Structurally, it can be characterized as a collagen/lectin hybrid. Together with SP-B, SP-A is required for conversion of secreted endogenous surfactant to tubular myelin in the alveolar lining. It also regulates surfactant secretion and reuptake of surfactant lipids by type II cells; these functions are probably receptor mediated. SP-D, a 12-mer of 39 kDa polypeptide chains, is a collagenous glycoprotein with structural similarities to C-type lectins. Both SP-A and SP-D stimulate alveolar macrophages. SP-B is a 79-residue polypeptide that contains three intrachain disulphide bridges. It exists mainly as a homodimer, which is strongly positively charged and may selectively remove anionic and unsaturated lipid species from the alveolar surface film, thereby increasing surface pressure. SP-C is a mainly alpha-helical, extraordinarily hydrophobic polypeptide containing 35 amino acid residues and covalently linked palmitoyl groups. Its alpha-helical portion is inserted into surfactant lipid bilayers. SP-C accelerates the adsorption of lipid bilayers to an interfacial monolayer. In babies with respiratory distress syndrome, the clinical response to treatment with surfactant containing SP-B and SP-C is much faster than in babies treated with protein-free synthetic surfactant. We speculate that, in the near future, surfactant preparations based on recombinant hydrophobic proteins will be available for clinical use.

Glycoproteins↗
PubMed1994

The innervation of the splenic capsule in the guinea pig: an immunohistochemical and ultrastructural study.

The innervation of the capsule of the guinea pig spleen was studied by light microscopy using an indirect fluorescent-labelled antibody technique, as well as by electron microscopy. A dense network of nerve fibres immunoreactive to the general neuronal marker, protein gene product 9.5 was observed in tangential sections through the capsule corresponding to the subcapsular compartment. The PGP 9.5-immunoreactivity in the fibres appeared to a large extent to be colocalised with tyrosine hydroxylase and neuropeptide Y (NPY) immunoreactivities as well as with synaptophysin immunoreactivity. Only very occasional fibres with substance P or calcitonin-gene-related peptide immunoreactivity were observed in tangential sections of the capsular region. By electron microscopy unmyelinated nerve fibres in the capsule were found to contain a large number of small dense-cored as well as clear vesicles and large dense-cored vesicles in varicose parts of the axons. The axolemma of the varicose regions was often naked, devoid of Schwann cells, and sometimes appeared denser than the nonspecialised parts of the membrane. These naked regions were observed in single sections to be apposed to splenic cells with variable intervals of extracellular space and interposed basal lamina material. Another type of contact was characterised by a very close association with splenic cells with no basal lamina interposed between the plasma membranes of the axon and the splenic cell. An intimate ultrastructural relationship was often also seen between varicose vesicle-containing axons and neighbouring axons in the nerve fibre bundles. The results show that the splenic capsule and its immediate neighbouring regions are innervated by catecholaminergic, NPY-containing fibres, which appear to establish different types of relations with the splenic cells as well as with one another.

Animals↗
PubMed1994

Effects of selective alfa 1 and beta 1-adrenoreceptor blockade on lipoprotein and carbohydrate metabolism in hypertensive subjects, with special emphasis on insulin sensitivity.

The central role of insulin resistance in patients with essential hypertension was the impetus for the present study, in which carbohydrate and lipid metabolism were examined before and after three months treatment with doxazosin (n = 14) and atenolol (n = 15). After completion of a randomised parallel group trial, the study was extended in a subgroup of the patients who continued treatment with doxazosin for a further nine months (n = 18). Insulin sensitivity was measured with the euglycemic hyperinsulinaemic clamp. Blood glucose and plasma insulin were analysed in the fasting state and during an intravenous glucose tolerance test (IVGTT). Lipoprotein fractions were analysed in serum. After three months, SBP and DBP in the standing position decreased to the same extent after the two drugs whereas the decrease in supine SBP did not reach statistical significance in the doxazosin group. Doxazosin, in contrast to atenolol, decreased serum triglycerides (-17%, P < 0.04) by lowering the VLDL and LDL fractions. Serum cholesterol fell after doxazosin (-7%, P < 0.02) but not after atenolol. The effects of doxazosin on serum lipids remained the same during the long-term follow-up. At three months neither drug had significantly affected variables reflecting insulin sensitivity although atenolol tended to decrease the insulin sensitivity index (-17%, P = 0.08). After 12 months the doxazosin group showed a significant increase in the insulin sensitivity index and a significant decrease in both basal plasma insulin and in the late insulin response at IVGTT.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗