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Biomedical subjects

A Jadhav

Publications and source records attributed to A Jadhav.

14 recordsLinked to original sources
PubMed2000

Diet-induced change in fatty acid composition of plasma triacylglycerols is not associated with change in glucagon-like peptide 1 or insulin sensitivity in people with type 2 diabetes.

BACKGROUND: Polyunsaturated fatty acids (PUFAs) and monounsaturated fatty acids (MUFAs) have been shown to positively affect blood lipids; however, their comparative effects on insulin sensitivity are unclear. OBJECTIVE: Our objective was to investigate whether chronic intake of MUFAs or PUFAs improves insulin sensitivity in people with type 2 diabetes via stimulation of the endogenous gut hormone glucagon-like peptide 1 [7-36] amide (GLP-1). DESIGN: Nine overweight people with type 2 diabetes received isoenergetic high-MUFA (20.3 +/- 3.5% of total energy) or high-PUFA (13.4 +/- 1. 3%) diets for 24 d in a randomized, double-blind crossover design. RESULTS: Weight and glycemic control remained stable throughout the study. Despite a significant change in the plasma triacylglycerol linoleic-oleic acid ratio (L:O) with both diets (MUFA: from 0.46 +/- 0.03 to 0.29 +/- 0.02, P: < 0.005; PUFA: from 0.36 +/- 0.04 to 0.56 +/- 0.05, P: < 0.05) and the phospholipid L:O (1.7 +/- 0.1 to 2.0 +/- 0.3; P: = 0.04) during consumption of the PUFA diet, this change was not associated with a change in insulin sensitivity, measured by the short-insulin-tolerance test. There was a significant reduction in the ratio of total to HDL cholesterol during consumption of the PUFA diet (5.2 +/- 0.4 compared with 4.7 +/- 0.3; P: = 0.005) but no change with the MUFA diet. There was no change in the fasting or postprandial incremental area under the curve in response to an identical standard test meal for glucose, insulin, triacylglycerol, nonesterified fatty acids, or GLP-1. CONCLUSIONS: Over the 3-wk intervention period, diet-induced change in the triacylglycerol or phospholipid L:O was not associated with either increased stimulation of GLP-1 or a change in insulin sensitivity in people with type 2 diabetes.

Blood Glucose↗
PubMed2000

Accessory soleus muscle as a cause of resistance to correction in congenital club foot: a case report.

A 14-month-old female with bilateral clubfeet was initially treated by serial casting and percutaneous tenotomy of the Achilles tendon, bilaterally. Both clubfeet subsequently underwent surgical treatment with a posteromedial release through a Cincinnati incision. At surgery on one clubfoot, an accessory Soleus muscle was found anterior to the Achilles tendon with a distinct insertion on the upper surface of calcaneus, anterior and medial to the insertion of Achilles tendon. This accessory Soleus muscle may have been the cause of resistance to correction in this congenital clubfoot.

Abnormalities, Multiple↗
PubMed1998

HMG-CoA reductase is not the site of the primary defect in phytosterolemia.

Phytosterolemia is an autosomal recessive disorder characterized by the excessive absorption, reduced excretion, and consequent high tissue and plasma levels of plant sterols, by the presence of tendon xanthomas, and by premature atherosclerosis. Low HMG-CoA reductase (HRase) activity and mass have been reported in liver and mononuclear leucocytes and low mRNA levels in liver from phytosterolemic subjects. These results led to the proposal that the primary defect in this condition involves the HRase gene locus. We examined this hypothesis in phytosterolemic subjects and heterozygous parents from four unrelated families. A variable number tandem repeat (VNTR) polymorphism of the HRase gene in the three informative families and a ScrFI restriction fragment length polymorphism (RFLP) within intron 2 of the gene in one of these families, segregated independently of the disease phenotype. Biological parentage was confirmed in the family in whom both polymorphisms failed to segregate with the disorder. These results conclusively exclude the HRase gene locus as the site of the primary defect in phytosterolemia. The study was extended by examining plasma levels of mevalonic acid and lathosterol, both markers of cholesterol biosynthesis, in response to cholestyramine, a bile acid sequestrant that is known to up-regulate HRase. Oral administration of cholestyramine resulted in a substantial (7.7-fold) increase in mevaIonic acid levels in two phytosterolemic subjects, compared with a 2.2-fold rise in their obligate heterozygote parents and a 2.3-fold increase in three healthy control subjects. The lathosterol/cholesterol (L/C) ratio showed a quantitatively similar response. Baseline levels of mevalonate and the L/C ratio were low in the phytosterolemic patients in conformity with reports of reduced cholesterol biosynthesis and HRase activity in this disorder. These functional data provide support for the concept that the primary defect in phytosterolemia does not affect a trans gene locus responsible for the constitutive expression or regulation of HMG-CoA reductase.

Adolescent↗
PubMed1988

Behavior of human apolipoprotein A-I: phospholipid and apoHDL:phospholipid complexes in vitro and after injection into rabbits.

Apolipoprotein A-I was purified from human high density lipoprotein and complexed with polyunsaturated phosphatidylcholine (PC) in deoxycholate (Lipostabil); the bile salt was removed subsequently by dialysis. The behavior of the resultant apoA-I/PC complexes was compared with that of Lipostabil in vitro and after injection into rabbits. In vivo apoA-I/PC complexes had the density of HDL throughout but had both alpha and pre beta electrophoretic mobility, the latter probably reflecting dissociation of apoA-I from PC. Lipostabil initially behaved like LDL but gradually acquired the density of HDL after incubation with plasma and in vivo. Both preparations increased plasma total phospholipids in normolipidemic rabbits to a similar extent, but, increments in HDL phospholipid were greater after apoA-I/PC complexes were injected. ApoHDL/PC complexes, prepared in a similar manner, appeared to promote efflux of cholesterol from perfused rabbit aortas in the presence of lecithin:cholesterol acyltransferase (LCAT) activity, consistent with a stimulatory effect on cholesterol mobilization. Injection of apoHDL/PC complexes into hyperlipidemic rabbits decreased plasma cholesterol but increased HDL cholesterol, whereas Lipostabil decreased both. These findings suggest that human apoA-I/PC complexes resemble HDL in their behavior more closely than does Lipostabil, and show that both types of liposome undergo modification upon interaction with plasma. It remains to be shown whether they possess any therapeutic potential.

Animals↗
PubMed1985

Failure of experimental atherosclerosis to sensitize coronary arteries to spasm in hypercholesterolemic rabbits.

Since hypercholesterolemia sensitizes isolated rabbit coronary arteries to vasoconstrictor stimuli, we assessed the possibility of reproducing occlusive coronary spasm both in vitro and in vivo in atherosclerotic rabbits. In Langendorff-perfused hearts from nine atherosclerotic rabbits (2% cholesterol diet for 18 weeks), despite a threefold increase of cholesterol concentration in the coronary wall compared with nine control rabbits, ergonovine and serotonin did not produce any increase of coronary vascular resistances; the increase produced by pitressin was significantly less in atherosclerotic than in normal hearts (56 +/- 13% vs 138 +/- 28%, p less than 0.05, respectively), whereas that produced by phenylephrine was similar (10.1 +/- 1.8% vs 8.5 +/- 2.4%, p = n.s.). In eight other unanesthetized rabbits we recorded the ECG during ergonovine administration (0.05 mg/kg) and during hypothalamic stimulation before and at regular intervals during the 2% cholesterol diet; rabbits survived for periods ranging from 1 to 22 weeks (mean 9.6 weeks). Only one animal had ST depression during episodes of marked tachycardia; no ischemic ECG changes were ever observed in the other rabbits despite the diffuse subintimal coronary deposition of cholesterol found postmortem. Thus, in atherosclerotic rabbits with chronic marked hypercholesterolemia, coronary arteries do not develop occlusive coronary spasm as observed in patients with variant angina.

Animals↗
PubMed1981

Superiority of partial ileal bypass over cholestyramine reducing cholesterol in familial hypercholesterolaemia.

Low density lipoprotein (LDL) turnover studies were conducted on three occasions in each of six patients with heterozygous familial hypercholesterolaemia (FH)-on diet, after 1 month on cholestyramine 16 g/day, and 2 months after partial ileal bypass. Partial ileal bypass lowered total and LDL cholesterol levels and increased the fractional catabolic rate of LDL to a greater extent than did cholestyramine; this difference presumably reflects the greater increase in bile acid excretion induced by the surgical procedure. Studies in two other heterozygotes showed that partial ileal bypass specifically enhanced receptor-mediated catabolism of LDL. The findings support the concept that therapeutic stimulation of bile acid synthesis increases the rate of receptor-mediated uptake and degradation of LDL by the liver.

Adult↗
PubMed1981

Defects of receptor-mediated low density lipoprotein catabolism in homozygous familial hypercholesterolemia and hypothyroidism in vivo.

The role of low density lipoprotein (LDL) receptors in the pathogenesis of hereditary and acquired forms of hypercholesterolemia has been investigated in vivo by simultaneously determining total and receptor-independent LDL catabolism with 125I-labeled LDL and 131I-labeled LDL coupled with cyclohexanedione. Receptor-mediated catabolism of LDL, determined as the difference between the turnover of 125I and 131I, was found to be virtually absent in two homozygotes with familial hypercholesterolemia and markedly reduced in a hypothyroid patient. Treatment of the latter with L-thyroxine markedly stimulated receptor-mediated catabolism and reduced LDL levels as did cholestyramine administration in a control subject. Reduction of LDL levels by plasma exchange in a control subject and homozygote had no such effect. These results demonstrate the existence of an intrinsic and almost total defect of receptor-mediated LDL catabolism in homozygous familial hypercholesterolemia and demontrate an analogous but reversible abnormality in hypothyroidism.

Biological Transport↗
PubMed1976

Effects of intravenous phospholipid on low density lipoprotein turnover in man.

The mechanism of the rise in plasma low density lipoprotein (LDL) levels following intravenous administration of a triglyceride-phospholipid emulsion (Intralipid) has been investigated by measuring LDL turnover in eight healthy subjects. The plasma half-life, and the absolute and fractional catabolic rates of LDL protein (apo-LDL) were unaffected by intragastric Intralipid, whereas apo-LDL half-life was prolonged and its fractional catabolic rate was decreased by intravenous Intralipid. Similar changes were observed after intravenous administration of the egg phospholipid constituent of Intralipid. Accompanying increases in the oleate: linoleate ratio of both high and low density lipoprotein cholesterol esters were secondary to phospholipid exchange between infused and endogenous lecithin. These results suggest that the increased concentration of LDL in plasma following intravenous administration of egg phospholipid-containing emulsions was due, at least in part, to a decrease in the fractional catabolic rate of apo-LDL. The data further suggest a possible relationship between apo-LDL catabolism and the fatty acid composition of LDL.

Apoproteins↗
PubMedDate not supplied

Plasma exchange and low density lipoprotein apheresis in Watanabe heritable hyperlipidemic rabbits.

Comparison of the effects of plasma exchange using lipoprotein-deficient plasma with those of LDL apheresis using a dextran sulphate column was undertaken in two groups of Watanabe heritable hyperlipidemic rabbits pre-labelled with 3H-cholesterol. Total and HDL cholesterol were reduced more by plasma exchange but HDL cholesterol rebounded higher after LDL apheresis; rises in HDL cholesterol correlated with preceding decreases in both HDL and total cholesterol. An increase in the specific activity of HDL cholesterol occurred on the day after each procedure, being more marked after plasma exchange, and was accompanied by a decrease in the cholesterol/phospholipid ratio of HDL. These results suggest that an influx of extravascular HDL into plasma occurred after both procedures, resulting in mobilization of tissue cholesterol.

Animals↗
PubMedDate not supplied

Rod diameter prediction in patients with osteogenesis imperfecta undergoing primary osteotomy.

SUMMARY: Because the cross-sectional shape of the long bones of patients with osteogenesis imperfecta is often elliptical, the use of preoperative radiographs to determine intramedullary rod diameter in these patients undergoing osteotomy may be misleading. To investigate this, the authors correlated the narrowest inner bone diameter (NID) on preoperative radiographs to the rod diameter (RD) on postoperative radiographs. The authors evaluated 79 bones in 27 patients undergoing primary osteotomy with intramedullary fixation. Only 5% of the bones had an equal NID and RD, with 81% of bones having a smaller RD than the measured NID. Although a positive correlation was found between RD and NID (correlation coefficient 0.76), measurement of the NID on preoperative radiographs did not provide a good prediction of the actual RD used in this series of children with osteogenesis imperfecta.

Adolescent↗