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Y Iizuka

Publications and source records attributed to Y Iizuka.

At least 37 records · Page 2Linked to original sources
PubMed2001

Effects of retinal glial cells on isolated rat retinal ganglion cells.

PURPOSE: The effect of retinal glial cells on retinal ganglion cell (RGC) survival was investigated in cocultures of pure, isolated retinal glial cells with pure, isolated RGCs. METHODS: RGCs from 2-day-old rats were cocultured for 48 hours, avoiding direct contact between cell types, with either nonconfluent retinal glial cells from 3-day-old rats or confluent retinal glial cells from 3-day-old, 12-day-old, or 1-year-old rats. Survival of RGCs was evaluated by flow cytometry. Amino acids were determined in culture medium. The effects of glutamate antagonists, 6-cyano-7-nitroquinoxaline-2,3-dione and MK801, a nitric oxide (NO) scavenger, 2-(4-carboxyphenyl)-4,4,5,5tetramethylimidazoline-1-oxyl-3-oxide potassium salt (c-PTIO), and an NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), were examined. RESULTS: Nonconfluent retinal glial cells significantly reduced the survival of small and large RGCs, but confluent retinal glial cells reduced the survival of only small RGCs, regardless of the rat's age at the time of retinal glial cell harvesting. Profiles of some amino acids significantly varied, depending on the culture condition. Cocultures of RGCs with nonconfluent retinal glial cells released significantly more glutamate into the medium than cocultures of RGCs with confluent retinal glial cells or RGCs in pure culture. The glutamate antagonists improved the survival of RGCs cocultured with nonconfluent retinal glial cells, especially when the two were administered in combination, and in the case of large RGCs. c-PTIO and L-NAME, also improved the survival of RGCs cocultured with nonconfluent retinal glial cells. CONCLUSIONS: Adverse effects of retinal glial cells on the survival of RGCs varied by size of the RGCs and retinal glial cell confluence. Glutamate and NO may be involved in retinal glial cell-related antisurvival effects.

Animals↗
PubMed2000

Roles of selenium in endotoxin-induced lipid peroxidation in the rats liver and in nitric oxide production in J774A.1 cells.

We examined the role of selenium (Se) in the mechanism of oxidative stress caused by endotoxin by feeding rats deficient a diet in this element. In rats fed the Se-deficient diet (concentration of Se, less than 0.027 microg g(-1)) for 10 weeks, Se level and glutathione peroxidase (GSH-Px) activity in the liver were about 47 and 43% lower, respectively, than those in rats fed a Se-adequate diet (Se, 0.2 microg g(-1)). Rat fed the Se-deficient diet and given endotoxin (6 mg kg(-1), i.p.) showed a mortality rates of about 43% at 18 h. Nevertheless, no lethality was observed with endotoxin (4 mg kg(-1), i.p.) challenge. Levels of serum lactate dehydrogenase and acid phosphatase leakage were significantly higher in Se-deficient rats than those in Se-adequate diet 18 h after endotoxin (4 mg kg(-1), i. p.) challenge. Superoxide anion generation and lipid peroxide formation in the liver of Se-deficient rat were markedly increased 18 h after endotoxin (4 mg kg(-1), i.p.) injection compared with those in the endotoxin/Se-adequate diet group, whereas non-protein sulfhydryl level in the liver after administration of endotoxin to Se-deficient rats was lower than that in Se-adequate rats treated with endotoxin. We investigated whether Se can suppress nitric oxide (NO) generation and cytotoxicity in endotoxin-treated J774A.1 cells. Treatment with Se (10(-6) M) markedly inhibited endotoxin (0.1 microg ml(-1))-induced NO production in J774A.1 cells. Se induced an increased activity of GSH-Px in cells after 24 h of incubation, suggesting that the preventive effect of Se on NO production in endotoxemia is due to the induction of Se-GSH-Px activity. However, Se did not affect endotoxin-induced cytotoxicity in J774A.1 cells. These findings suggested that the oxidative stress caused by endotoxin may be due, at least in part, to changes in Se regulation during endotoxemia.

Animals↗
PubMed2000

Sterol regulatory element-binding protein-1 is regulated by glucose at the transcriptional level.

In vivo studies suggest that sterol regulatory element-binding protein (SREBP)-1 plays a key role in the up-regulation of lipogenic genes in the livers of animals that have consumed excess amounts of carbohydrates. In light of this, we sought to use an established mouse hepatocyte cell line, H2-35, to further define the mechanism by which glucose regulates nuclear SREBP-1 levels. First, we show that these cells transcribe high levels of SREBP-1c that are increased 4-fold upon differentiation from a prehepatocyte to a hepatocyte phenotype, making them an ideal cell culture model for the study of SREBP-1c induction. Second, we demonstrate that the presence of precursor and mature forms of SREBP-1 protein are positively regulated by medium glucose concentrations ranging from 5. 5 to 25 mm and are also regulated by insulin, with the amount of insulin in the fetal bovine serum being sufficient for maximal stimulation of SREBP-1 expression. Third, we show that the increase in SREBP-1 protein is due to an increase in SREBP-1 mRNA. Reporter gene analysis of the SREBP-1c promoter demonstrated a glucose-dependent induction of transcription. In contrast, expression of a fixed amount of the precursor form of SREBP-1c protein showed that glucose does not influence its cleavage. Fourth, we demonstrate that the glucose induction of SREBP could not be reproduced by fructose, xylose, or galactose nor by glucose analogs 2-deoxy glucose and 3-O-methyl glucopyranose. These data provide strong evidence for the induction of SREBP-1c mRNA by glucose leading to increased mature protein in the nucleus, thus providing a potential mechanism for the up-regulation of lipogenic genes by glucose in vivo.

Animals↗
PubMed2000

Promoter analysis of the mouse sterol regulatory element-binding protein-1c gene.

Recent data suggest that sterol regulatory-binding protein (SREBP)-1c plays a key role in the transcriptional regulation of different lipogenic genes mediating lipid synthesis as a key regulator of fuel metabolism. SREBP-1c regulates its downstream genes by changing its own mRNA level, which led us to sequence and analyze the promoter region of the mouse SREBP-1c gene. A cluster of putative binding sites of several transcription factors composed of an NF-Y site, an E-box, a sterol-regulatory element 3, and an Sp1 site were located at -90 base pairs of the SREBP-1c promoter. Luciferase reporter gene assays indicated that this SRE complex is essential to the basal promoter activity and confers responsiveness to activation by nuclear SREBPs. Deletion and mutation analyses suggest that the NF-Y site and SRE3 in the SRE complex are responsible for SREBP activation, although the other sites were also involved in the basal activity. Gel mobility shift assays demonstrate that SREBP-1 binds to the SRE3. Taken together, these findings implicate a positive loop production of SREBP-1c through the SRE complex, possibly leading to the overshoot in induction of SREBP-1c and its downstream genes seen in the livers of refed mice. Furthermore, reporter assays using larger upstream fragments indicated another region that was inducible by addition of sterols. The presence of the SRE complex and a sterol-inducible region in the same promoter suggests a novel regulatory link between cholesterol and fatty acid synthesis.

Animals↗
PubMed2000

Absence of ACAT-1 attenuates atherosclerosis but causes dry eye and cutaneous xanthomatosis in mice with congenital hyperlipidemia.

Acyl-CoA:cholesterol acyltransferase (ACAT) catalyzes esterification of cellular cholesterol. To investigate the role of ACAT-1 in atherosclerosis, we have generated ACAT-1 null (ACAT-1-/-) mice. ACAT activities were present in the liver and intestine but were completely absent in adrenal, testes, ovaries, and peritoneal macrophages in our ACAT-1-/- mice. The ACAT-1-/- mice had decreased openings of the eyes because of atrophy of the meibomian glands, a modified form of sebaceous glands normally expressing high ACAT activities. This phenotype is similar to dry eye syndrome in humans. To determine the role of ACAT-1 in atherogenesis, we crossed the ACAT-1-/- mice with mice lacking apolipoprotein (apo) E or the low density lipoprotein receptor (LDLR), hyperlipidemic models susceptible to atherosclerosis. High fat feeding resulted in extensive cutaneous xanthomatosis with loss of hair in both ACAT-1-/-:apo E-/- and ACAT-1-/-:LDLR-/- mice. Free cholesterol content was significantly increased in their skin. Aortic fatty streak lesion size as well as cholesteryl ester content were moderately reduced in both double mutant mice compared with their respective controls. These results indicate that the local inhibition of ACAT activity in tissue macrophages is protective against cholesteryl ester accumulation but causes cutaneous xanthomatosis in mice that lack apo E or LDLR.

Animals↗
PubMed2000

Prognostic factors in the surgical treatment of ruptured abdominal aortic aneurysms.

Although the operative mortality following elective aneurysmectomy has achieved satisfactory results, that following surgery for ruptured abdominal aortic aneurysms (AAAs) remains high. The purpose of this study was to identify the factors affecting the mortality rate associated with the treatment of ruptured AAAs. Between 1978 and 1999, 33 patients underwent emergency surgery for a ruptured AAA. The operative mortality was 33.3% and in-hospital mortality was 6.0%. Hypotension, defined as a systolic blood pressure <80 mmHg, was seen in 19 patients at the time of presentation, 9 of whom underwent surgery in this state. In the remaining 10 patients, it was possible to increase the systolic blood pressure to > or =80 mmHg preoperatively. Of the 11 patients who died within 30 days of surgery, 9 had hypotension at the time of induction of anesthesia and only 2 had a systolic blood pressure of > or =80 mmHg. A satisfactory outcome was achieved in patients whose condition met the following criteria: a systolic blood pressure > or =80 mmHg at the time of operation, minimal aortic cross-clamping time, less blood loss and blood transfusions, and a shorter operation time to repair the ruptured AAA. Concomitant heart disease was also found to be an important prognostic factor.

Adult↗
PubMed2000

Vacuolated cell mesothelioma of the pericardium resembling liposarcoma: a case report.

We report a case of localized pericardial mesothelioma with unusual histological features in a 44-year-old woman. Her radiological imagings showed an 11-cm pericardial tumor, between the heart and aortic arch. Microscopically, the tumor was predominantly composed of vacuolated cells and vaguely reminiscent of well differentiated "lipoma-like" liposarcoma, but only small foci of the tumor showed the papillotubular configuration. Histochemically, the tumor cells contained hyaluronic acid in the vacuoles but no lipids. Immunohistochemically, they showed immunoreactivity for cytokeratin, calretinin, vimentin, and epithelial membrane antigen. Ultrastructural study showed that the vacuoles of the tumor cells were intracytoplasmic lumina. The intracytoplasmic lumina and the surface membranes of the tumor cells had many long and slender microvilli with focal bush-like appearance. Desmosomes between adjacent cells were occasionally observed. To our knowledge, this is the first case report of epithelial type mesothelioma predominantly composed of vacuolated tumor cells, microscopically mimicking liposarcoma.

Adult↗
PubMed2000

Neutralization of prostaglandin E1 intravenous solution reduces infusion phlebitis.

Previous studies have shown moderate or severe phlebitis at the site of venipuncture in some patients who receiving prostaglandin E1 (PGE1) infusion therapy. Such phlebitis is sometimes severe enough to necessitate the cessation of PGE1 therapy. This study investigated how to continue PGE1 infusion therapy for 3 weeks with tolerable phlebitis. Although a 60 microg dose of PGE1 is usually dissolved in 500 mL of fluid to avoid phlebitis, we used 200 mL to prevent volume overload. This PGE1 solution was neutralized to pH 7.4 with 4 mL of 7% sodium bicarbonate. We examined the frequency and severity of phlebitis among patients who received a 2-h PGE1 infusion twice daily. Eighteen patients who were hospitalized for peripheral vascular disease between June 1998 and May 1999 were studied. All of them were men and their mean age was 63.3 +/- 8.9 years (range: 47-78 years). Fourteen patients had arteriosclerosis obliterans and four had Buerger's disease. When the severity of phlebitis was determined according to Dinley's criteria, two patients (11%) had grade 0, four patients (22%) had grade 1, eleven patients (61%) had grade 2, and one patient (6%) had grade 3 phlebitis. Usually, PGE1 infusion therapy is stopped when phlebitis reaches grade 4 or more, but there were no such cases in this study. We also found that aging was significantly correlated with a decrease in the severity of phlebitis (Spearman's rank correlation test: r = -0.545, p = 0.0193).

Adult↗
PubMed2000

Midline lateralization thyroplasty for adductor spasmodic dysphonia.

Midline lateralization thyroplasty was successfully performed on a patient with adductor spasmodic dysphonia. The thyroid cartilage was incised at the midline, and a 3 x 2-mm perforation was made at the anterior commissure to widen it. The perforation was closed with a free composite graft taken from the upper edge of the thyroid ala, and the incised thyroid cartilage edges were kept separated 4 mm apart with silicone wedges. A part of the sternohyoid muscle was rotated to seal any leak from the perforation. The postoperative course was uneventful. The voice has been restored to normal, and there is no sign of recurrence of the symptom so far, as of 1 year 5 months postoperative. Although a longer follow-up is needed, this case indicates that midline type II thyroplasty could be a useful treatment for adductor spasmodic dysphonia.

Adult↗
PubMed2000

A Japanese patient with lipoprotein lipase deficiency homozygous for the Gly188Glu mutation prevalent worldwide.

We studied the molecular basis of familial lipoprotein lipase (LPL) deficiency in a new Japanese kindred. The proband was a four-month-old infant with severe hyperchylomicronemia. In postheparin plasma, LPL activity was virtually absent, although LPL mass was detectable. Single strand conformational polymorphism (SSCP) analysis showed an abnormal band with exon 5 of the LPL gene that was amplified by PCR from the proband's genomic DNA. DNA sequence analysis of the amplified fragment demonstrated that the proband was homozygous for a G-to-A change at nucleotide position 818 resulting in the substitution of glutamic acid for glycine at codon 188. Although this is among the first Gly188Glu mutations identified in Japanese, the missense mutation has previously been reported as a prevalent cause of familial LPL deficiency worldwide and has been proposed to have a common origin. However, DNA haplotype analysis with either restriction fragment length polymorphism (RFLP) or microsatellite markers revealed that the DNA haplotype of the proband was not identical to the haplotype previously reported as common to the other patients with the Gly188Glu mutation. These results add the Gly188Glu mutation to the growing list of LPL gene mutations underlying familial LPL deficiency in Japanese and indicate that the origin of the Gly188Glu mutation is not necessarily common but would be multicentric at least in part.

Adult↗
PubMed2000

[Endovascular neurointervention for cerebral aneurysm].

Embolization would have an advantage in the treatment of cerebral aneurysms by eliminating the need for craniotomy. The recent protocol of endovascular treatment for cerebral aneurysm is classified into two main categories; is parent artery occlusion and intra-aneurysmal embolization. For aneurysms with a broad neck and large sac, it is recommended to consider proximal arterial occlusion if tolerance is confirmed by cerebral blood flow study at the time of balloon Matas' test. Parent artery occlusion is a classical technique, but still mandatory and effective clinically. In patients who have aneurysms with a has well-defined neck and who are not good candidates for craniotomy, intra-aneurysmal embolization would be recommended as an alternative means of treatment. Care should be taken to prevent problems and complications, including careful catheter and guidewire manipulation. Careful selection of cases and appropriate pre-, intra-, and post-procedure patient management is essential. Since the clinical application of Gugliemi's detachable coil (GDC) started, the potential of endovascular treatment for cerebral aneurysm has changed considerably. Preliminary results of embolization using GDC suggest that endovascular treatment would offer marked improvement in the management of patients harboring cerebral aneurysms.

Embolization, Therapeutic↗
PubMed2000

[Endovascular neurointervention for intracranial dural arteriovenous fistula].

Dural arteriovenous fistula(DAVF) is an abnormal shunt within the dura matter or near the venous sinuses. Various congenital and idiopathic causes have been suggested, including such as venous sinus occlusion, trauma, surgery, and changes in hormone levels, but the exact etiology of the disease is unknown. The pattern of venous drainage seen on angiography was used as the basis for a classification of DAVF by Djindjian. Recent classification suggests that lesions that drain into the venous sinus or meningeal vein will behave only in a benign manner, whereas those that have subarachnoid venous drainage or alone or in addition will behave aggressively. Selection of treatment can be made from observation, carotid manual compression, transarterial or transvenous embolization, radiotherapy, or surgical intervention. The goal of treatment and consequently the techniques used, depends on the intensity of symptoms or the neurologic and, in particular, hemorrhagic risk posed by the type of venous drainage. The therapeutic decision depends also on the patient's general clinical status. Embolization can create a reduction of flow, which results in disappearance in symptoms and sometimes complete cure as seen at angiography. Complex DAVF must be treated with combined endovascular techniques plus neurosurgery or radiotherapy.

Arteriovenous Fistula↗
PubMed2000

Biological markers of alcoholism with respect to genotypes of low-Km aldehyde dehydrogenase (ALDH2) in Japanese subjects.

BACKGROUND: Although the mutant low-Km acetaldehyde dehydrogenase (ALDH2) allele (ALDH2(2)) with reduced capacity to metabolize acetaldehyde offers biological protection against alcoholism and subsequent alcohol-induced organ damage in many individuals, a significant proportion of individuals with heterozygote of the normal and mutant ALDH2 gene (ALDH2(1)/2(2)) consume excessive amounts of alcohol. Indeed, it has been postulated that habitual drinkers with ALDH2(1)/2(2) may be at a higher risk for alcoholic liver disease than those with ALDH2(1)/2(1). In this study, we determined how representative biological markers of alcoholism (gamma-glutamyltransferase [GGT], carbohydrate-deficient transferrin [CDT], and the mean corpuscular volume of erythrocytes [MCV]) differ with respect to the ALDH2 genotypes in Japanese habitual drinkers. METHODS: We obtained genomic DNA samples from 227 Japanese men with various drinking habits. ALDH2 genotypes were determined by allele-specific polymerase chain reaction. GGT, CDT, and MCV were determined and compared between ALDH2(1)/2(1) and ALDH2(1)/2(2) habitual drinkers who consumed more than 66 g of alcohol per day for more than 5 years. We measured CDT by anion-exchange chromatography followed by turbidity immunoassay by using a commercially available assay kit (Axis %CDT TIA). RESULTS: CDT levels were comparable between the two groups. GGT activities were significantly greater in ALDH2(1)/2(1) than in ALDH2(1)/2(2) habitual drinkers (81 +/- 85 vs. 53 +/- 40 IU/liters, p < 0.02). MCV values, on the other hand, were significantly larger in ALDH2(1)/2(2) than in ALDH2(1)/2(1) subjects (98.2 +/- 5.8 vs. 95.8 +/- 4.2 fl, p = 0.02). When we used elevation of either CDT or GGT to detect habitual drinking in ALDH2(1)/2(1) and 2(1)/2(2) subjects, the sensitivities were 57% and 46%, respectively. CDT levels were similar between habitual drinkers with normal aspartate aminotransferase levels and those with elevated levels. CONCLUSION: GGT and MCV, but not CDT, differ with respect to the ALDH2 genotypes in Japanese male habitual drinkers. ALDH2 genotypes should be considered when interpreting data on biological markers of alcoholism.

Adult↗
PubMed2000

Effects of brain-derived neurotrophic factor and neurotrophin-4 on isolated cultured retinal ganglion cells: evaluation by flow cytometry.

PURPOSE: Effects of brain-derived neurotrophic factor (BDNF) and neurotrophin (NT)-4 on retinal ganglion cells (RGCs) isolated and cultured in a serum-free medium are evaluated objectively by using flow cytometry. METHODS: RGCs from the retinas of 2-day-old rats were isolated in a two-step panning and cultured in a serum-free medium. BDNF (1, 10, and 100 pg/ml or 1, 10, and 100 ng/ml), NT-4 (0.1, 1, 10, and 100 ng/ml) or their vehicle, phosphate-buffered saline, were individually added to aliquots of the medium to be cultured for 48 hours. Then, after adding 5-chloromethylfluorescein diacetate, the survival of RGCs was evaluated using flow cytometry. RESULTS: The method used allowed the authors to analyze 10,000 RGCs per sample in approximately 2 minutes, so that a much larger number of cells was evaluated in a shorter period than with previously reported methods. RGCs were classified into either large or small RGCs, and the survival of each of these groups was determined objectively by the amount of fluorescent emission. BDNF improved the survival rate of RGCs concentration-dependently. In particular, the survival rate of small RGCs was greatly improved. BDNF at 100 ng/ml increased the survival rate of small RGCs by 17.4% and that of large RGCs by 7.8% in comparison to the controls. NT4 did not significantly improve the survival rates of either large or small RGCs. CONCLUSIONS: BDNF improved the survival rate of RGCs, particularly of small RGCs, concentration-dependently, but NT-4 had little influence on the survival rate. The current method was useful in evaluating the effects of neuroprotective factors or neurotoxic factors on cultured RGCs.

Animals↗
PubMed2000

Novel mutations in the microsomal triglyceride transfer protein gene causing abetalipoproteinemia.

Abetalipoproteinemia (ABL) is an inherited disease characterized by the virtual absence of apolipoprotein B (apoB)-containing lipoproteins from plasma. Only limited numbers of families have been screened for mutations in the microsomal triglyceride transfer protein (MTP) gene. To clarify the genetic basis of clinical diversity of ABL, mutations of the MTP gene have been screened in 4 unrelated patients with ABL. Three novel mutations have been identified: a frameshift mutation caused by a single adenine deletion at position 1389 of the cDNA, and a missense mutation, Asn780Tyr, each in homozygous forms; and a splice site mutation, 2218-2A-->G, in a compound heterozygous form. The frameshift and splice site mutations are predicted to encode truncated forms of MTP. When transiently expressed in Cos-1 cells, the Asn780Tyr mutant MTP bound protein disulfide isomerase (PDI) but displayed negligible MTP activity. It is of interest that the patient having the Asn780Tyr mutation, a 27-year-old male, has none of the manifestations characteristic of classic ABL even though his plasma apoB and vitamin E were virtually undetectable. These results indicated that defects of the MTP gene are the proximal cause of ABL.

Abetalipoproteinemia↗
PubMed1999

Sterol regulatory element-binding protein-1 as a key transcription factor for nutritional induction of lipogenic enzyme genes.

To elucidate the physiological role of sterol regulatory element-binding protein-1 (SREBP-1), the hepatic mRNA levels of genes encoding various lipogenic enzymes were estimated in SREBP-1 gene knockout mice after a fasting-refeeding treatment, which is an established dietary manipulation for the induction of lipogenic enzymes. In the fasted state, the mRNA levels of all lipogenic enzymes were consistently low in both wild-type and SREBP-1(-/-) mice. However, the absence of SREBP-1 severely impaired the marked induction of hepatic mRNAs of fatty acid synthetic genes, such as acetyl-CoA carboxylase, fatty acid synthase, and stearoyl-CoA desaturase, that was observed upon refeeding in the wild-type mice. Furthermore, the refeeding responses of other lipogenic enzymes, glycerol-3-phosphate acyltransferase, ATP citrate lyase, malic enzyme, glucose-6-phosphate dehydrogenase, and S14 mRNAs, were completely abolished in SREBP-1(-/-) mice. In contrast, mRNA levels for cholesterol biosynthetic genes were elevated in the refed SREBP-1(-/-) livers accompanied by an increase in nuclear SREBP-2 protein. When fed a high carbohydrate diet for 14 days, the mRNA levels for these lipogenic enzymes were also strikingly lower in SREBP-1(-/-) mice than those in wild-type mice. These data demonstrate that SREBP-1 plays a crucial role in the induction of lipogenesis but not cholesterol biosynthesis in liver when excess energy by carbohydrates is consumed.

Acetyl-CoA Carboxylase↗
PubMed1999

A crucial role of sterol regulatory element-binding protein-1 in the regulation of lipogenic gene expression by polyunsaturated fatty acids.

Dietary polyunsaturated fatty acids (PUFA) are negative regulators of hepatic lipogenesis that exert their effects primarily at the level of transcription. Sterol regulatory element-binding proteins (SREBPs) are transcription factors responsible for the regulation of cholesterol, fatty acid, and triglyceride synthesis. In particular, SREBP-1 is known to play a crucial role in the regulation of lipogenic gene expression in the liver. To explore the possible involvement of SREBP-1 in the suppression of hepatic lipogenesis by PUFA, we challenged wild-type mice and transgenic mice overexpressing a mature form of SREBP-1 in the liver with dietary PUFA. In the liver of wild-type mice, dietary PUFA drastically decreased the mature, cleaved form of SREBP-1 protein in the nucleus, whereas the precursor, uncleaved form in the membranes was not suppressed. The decreases in mature SREBP-1 paralleled those in mRNAs for lipogenic enzymes such as fatty acid synthase and acetyl-CoA carboxylase. In the transgenic mice, dietary PUFA did not reduce the amount of transgenic SREBP-1 protein, excluding the possibility that PUFA accelerated the degradation of mature SREBP-1. The resulting sustained expression of mature SREBP-1 almost completely canceled the suppression of lipogenic gene expression by PUFA in the SREBP-1 transgenic mice. These results demonstrate that the suppressive effect of PUFA on lipogenic enzyme genes in the liver is caused by a decrease in the mature form of SREBP-1 protein, which is presumably due to the reduced cleavage of SREBP-1 precursor protein.

Animal Feed↗