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H Inadera

Publications and source records attributed to H Inadera.

26 records · Page 2Linked to original sources

A missense mutation (Ala334-->Thr) in exon 7 of the lipoprotein lipase gene in a case with type I hyperlipidemia.

The patient is a 34-year-old female. Her fasting plasma triglyceride and cholesterol levels were 7523 mg/dl and 818 mg/dl, respectively, at 35 weeks' gestation. The lipoprotein lipase (LPL) activity and mass from postheparin plasma of the proband were 0.02 (normal range: 5.51 +/- 1.12 mu mol/ml/h) and 168 ng/ml (normal range: 220 +/- 42 ng/ml), respectively, indicating that the LPL of the patient would be functionally defective LPL. DNA sequence analysis of the LPL gene from the patient revealed a homozygous nucleotide change: a G--> A transition at nucleotide position of 1255 resulting in an amino acid substitution of Thr for Ala 334. This is the first natural missense mutation identified in exon 7 of the LPL gene.

Adult↗

Proliferation and triglyceride synthesizing activities of fibroblast-like cells derived from epididymal and subcutaneous adipose tissues of rats.

Fibroblast-like cells from subcutaneous adipose tissue and epididymal adipose tissue were prepared from rats and their proliferation and [14C]deoxy-glucose uptake and triglyceride synthesis from [14C]palmitate were investigated. The proliferation of fibroblast-like cells from subcutaneous adipose tissue was greater than that from epididymal adipose tissue. Insulin enhanced the proliferation of fibroblast-like cells derived from subcutaneous adipose tissue, but not from epididymal adipose tissue. The uptake of [14C]deoxy-glucose by fibroblast-like cells from the two sources was similar. Triglyceride synthesis from [14C]palmitate by epididymal fibroblast-like cells was higher than that by subcutaneous fibroblast-like cells. The [14C]deoxy-glucose uptake and triglyceride synthesis from [14C]palmitate by fibroblast-like cells from the two sources were not enhanced by the addition of insulin. These findings suggest the existence of different types of adipocytes in subcutaneous and epididymal adipose tissues in terms of proliferation, and show that the proliferation of fibroblast-like cells from subcutaneous adipose tissue is regulated by insulin. The triglyceride synthesis by immature adipocytes from both adipose tissues was not affected by insulin.

Adipose Tissue↗

Moderate oxidation of hypertriglyceridemic low-density lipoprotein causes apolipoprotein B epitope change and enhances its uptake by macrophages.

We prepared monoclonal antibody (MabB4) that selectively binds to acetylated low-density lipoprotein (LDL). Native hypertriglyceridemic LDL (HT-LDL) obtained from IIb and native normotriglyceridemic LDL (NT-LDL) from type IIa scarcely bound with MabB4. When these LDL were oxidized moderately by incubation with copper ions, the binding of MabB4 to HT-LDL was enhanced compared to that of NT-LDL, although the contents of the hydroperoxide they produced were the same. The incorporation of moderately oxidized HT-LDL into macrophages was enhanced compared to that of NT-LDL, and the rate of incorporation parallel the binding of LDL for MabB4. These results suggested that moderate oxidation of HT-LDL expressed some apolipoprotein B epitope on the surface of acetylated LDL to a much greater degree than NT-LDL, and that this expressed epitope might work as a ligand of moderately oxidized HT-LDL for the recognition by macrophages.

Apolipoproteins B↗

Type I hyperlipoproteinemia caused by lipoprotein lipase defect in lipid-interface recognition was relieved by administration of medium-chain triglyceride.

We have previously reported lipoprotein lipase with a defect of lipid-interface recognition in a patient with type I hyperlipoproteinemia. In this patient, lipoprotein lipase from post-heparin plasma (PHP) hydrolyzed monomeric substrate tributyrin, but scarcely hydrolyzed triolein emulsified with Triton X-100 and that in very-low-density lipoproteins ([VLDL] d < 1.006 g/mL), and did not bind to VLDL. The triglyceride (TG) level of this patient did not decrease to less than 1,000 mg/dL with a low-fat diet (1,400 kcal containing 10 g fat/d). When the patient took 30 g medium-chain TG (MCT) in addition to the 1,400-kcal diet, her serum TG level decreased to 250 mg/dL and her clinical signs improved. The low clearance rate of serum TG with heparin injection improved after intake of MCT. Caproic acid levels were maintained at 1.4% and 2.6% in chylomicrons and VLDL after MCT intake, respectively. The patient's lipoprotein lipase hydrolyzed triolein emulsified with 2% tricaprin at the same rate as that of control lipoprotein lipase. The patient's lipoprotein lipase-catalyzed hydrolyzing rate of triolein in chylomicrons obtained after MCT administration was also enhanced up to 70% of that of control lipoprotein lipase. These findings suggest that hypertriglyceridemia caused by lipoprotein lipase with a defect in lipid-interface recognition could be relieved with the administration of medium-chain TG, and that one of the mechanisms of this effect might be a modification of TG-rich lipoproteins by MCT.

Adolescent↗

Response of lipoprotein lipase to calorie intake in streptozotocin-induced diabetic rats.

The mechanism regulating lipoprotein lipase (LPL) expression in adipose tissue was examined in rats in the conditions of different calorie intakes with and without streptozotocin-induced (STZ-) diabetes. The LPL activity released from adipose tissue was greater with the higher calorie intake (20 g of normal chow diet per day) than with the lower calorie intake (13 g of normal chow diet per day), and was greater in normal rats than in STZ-diabetic rats. The LPL activity was proportional to the serum insulin level in all conditions. Dot-blot analysis showed that the amount of LPL mRNA in adipose tissue was increased by the higher calorie diet and that the increase was less in the diabetic state. Expression of mRNA was also nearly parallel with the serum insulin level. LPL activity released from the heart was not affected by either the calorie intake or the diabetic state. These results suggest that the mechanisms of LPL expression in adipose tissue and the heart are different, and that LPL expression in adipose tissue was closely dependent on the insulin level.

Adipose Tissue↗

Endocrine disorders and body fat distribution.

To evaluate the role of hormones in formation of regional fat distribution, the ratios of visceral fat (V) to subcutaneous fat (S) in the abdomen of rats with various endocrine disorders were determined by computer tomography. Abdominal fat index (AFI), which was obtained by ultrasonography, correlated with V/S. In Cushing's syndrome, seven out of nine patients showed visceral type and V/S ratio positively correlated with cortisol levels. In acromegaly, three out of four patients showed visceral type and V/S ratio correlated not only with growth hormone level, but also with insulin level. All three insulinoma patients showed visceral type. During pregnancy, AFI decreased at the late stage of pregnancy. These results suggest that in visceral fat formation, insulin is the most important factor, and estrogen is an important factor for subcutaneous formation. In vitro experiments showed that visceral fat was much more sensitive to insulin in terms of glucose uptake and triglyceride synthesis than visceral fat. Fibroblast-like cells derived from adipose tissue were cultured. Estrone enhanced cell growth of fibroblast-like cells derived from subcutaneous fat tissue more than that from visceral fat tissue. The results suggested that hyperinsulinism primarily promotes visceral fat tissue enlargement and that estrogen might promote subcutaneous fat tissue enlargement.

Acromegaly↗