Biomedical subjects

K Nagata

Publications and source records attributed to K Nagata.

At least 343 records · Page 19Linked to original sources

PubMed1997

Mechanism of apoptotic cell death of human gastric carcinoma cells mediated by transforming growth factor beta.

Human gastric carcinoma cell line HSC-39 has been shown to undergo apoptotic cell death in response to treatment with transforming growth factor beta1 (TGF-beta1). To understand better the cell death mechanism in this TGF-beta1-mediated apoptosis, we investigated the effect of the expression of TGF-beta-stimulated clone 22 (TSC-22) on cell death events. TGF-beta1 induced TSC-22 gene expression in HSC-39 cells only when the cells had previously been adapted to the serum-free culture conditions required to undergo TGF-beta1-mediated apoptosis. HSC-39 cells transfected with a TSC-22 expression vector showed a significant decrease in cell viability compared with those transfected with a control vector. The cellular events characteristic of apoptosis, chromatin condensation and DNA fragmentation were observed only in cells transfected with a TSC-22 expression vector. On immunostaining of the transfected cells, almost every cell that expressed TSC-22 tagged with influenza virus haemagglutinin exhibited the morphology of an apoptotic cell. Partial protection from the cell death effect of TGF-beta1 on HSC-39 cells was observed when cells were treated with acetyl-L-aspartyl-L-glutamyl-L-valyl-L-aspart-1-al (Ac-DEVD-CHO, an inhibitor specific for CPP32-type protease). Protection against cell death by the transfection of a TSC-22 expression vector was also offered by Ac-DEVD-CHO addition. These results suggest that TSC-22 elicits the apoptotic cell death of human gastric carcinoma cells through the activation of CPP32-like protease and mediates the TGF-beta1 signalling pathway to apoptosis.

Apoptosis↗

PubMed1997

Different thresholds in the responses of two heat shock transcription factors, HSF1 and HSF3.

Avian cells express three HSF genes encoding a unique factor, HSF3, as well as homologues of mammalian HSF1 and HSF2. HSF1 is the major factor that mediates the heat shock signal in mammalian cells. We reported previously that cHSF3, as well as cHSF1, is activated by heat shock in chicken cells. In this study, we examined the functional differences between cHSF1 and cHSF3. Comparison of the heat-inducible DNA binding activity of cHSF1 with cHSF3 at various temperatures revealed that the latter was activated at higher temperatures than the former. At a mild heat shock, such as 41 degrees C, only cHSF1 was activated, whereas both cHSF1 and cHSF3 were activated following a severe heat shock at 45 degrees C. Heat-inducible nuclear translocation and trimerization were accompanied by DNA binding activity. We also observed that cHSF3 was activated by treating cells with higher concentrations of sodium arsenite compared to cHSF1. The DNA binding activity of cHSF3 by severe heat shock lasted for a longer period than that of cHSF1. Interestingly, the total amount of cHSF3 increased only upon severe heat shock, whereas that of HSF1 decreased. Substantial amounts of cHSF3 remained in the soluble fraction under severe heat shock, whereas cHSF1 rapidly moved to the insoluble fractions in that conditions. Comparison of transcriptional activity of the activation domains of cHSF1 and cHSF3 revealed that the activity of cHSF3 was as strong as that of cHSF1. These findings indicate that there are different thresholds for cHSF1 and cHSF3 and that cHSF3 is involved in the persistent and burst activation of stress genes upon severe stress in chicken cells. Pretreatment of cycloheximide elevated the threshold concentrations of arsenite of both factors. This suggests that denaturation of nascent polypeptides could be the first trigger for the activation of both factors, and the pathways for activation of cHSF1 and cHSF3 may be identical, or at least share some common mechanisms.

Animals↗

PubMed1997

Oxygen-dependent regulation of the respiration and growth of Escherichia coli by nitric oxide.

To elucidate the role of nitric oxide (NO) in the metabolisms of enteric bacteria, its effect on the respiration and growth of Escherichia coli was examined. Respiration of E. coli was reversibly inhibited by NO particularly under low oxygen tensions. Growth of E. coli was also inhibited by NO more strongly under low oxygen tension than at its high concentration. Because the intestinal lumen is anaerobic, even a small amount of NO might strongly inhibit the energy metabolism and growth of E. coli and other enteric bacteria in vivo than in air atmospheric conditions in which oxygen tension is unphysiologically high.

Escherichia coli↗

PubMed1997

Roles of gamma-carboxylation and a sex hormone-binding globulin-like domain in receptor-binding and in biological activities of Gas6.

Gas6 is a ligand for an Axl/Sky receptor tyrosine kinase subfamily and has a structure composed of a Gla domain, four EGF-like domains and a C-terminal sex hormone-binding globulin (SHBG)-like domain. When examining the role of each domain in receptor-binding and biological activities of Gas6, we found that receptor-binding and mitogenic activities were markedly reduced by inhibiting gamma-carboxylation of the Gla domain, while a Gas6 mutant composed of only an SHBG-like domain retained both of these activities. Thus, the SHBG-like domain is apparently an entity indispensable for Gas6 activities, and gamma-carboxylation of the Gla domain has a regulatory role in retaining the activity of native Gas6.

3T3 Cells↗

PubMed1997

Arylamine activating sulfotransferase in liver.

Carcinogenic N-hydroxy-arylamines and -arylamides undergo metabolic activation by several enzymes in mammals to cause the DNA damage. Cytosolic sulfotransferases in rat and human livers, which belong to the ST1 (SULT1) family, have been studied to assess their properties to mediate the metabolic activation. A human orthologue of rat ST1C1 from, which catalyzes sulfation of N-hydroxy-2-acetylaminofluorene, was screened in a EMBL genomic library with ST1C1 cDNA [Nagata, K., S. Ozawa, M. Miyata, M. Shimada, D.-W. Gong, Y. Yamazoe and R. Kato (1993) J. Biol. Chem., 268, 24720-24725]. Sequencing of the hybridized clones indicate that at least 3'-terminal region of human ST1C1 orthologue contains sequence highly homologus to rat ST1C1 at both nucleotide and deduced amino acid levels. The experiments using anti-rat ST1C1 antibody and nucleotide probes for human ST1C1 showed no detectable band in Western blots and an mRNA-detecting method with polymerase chain reaction, respectively, in human liver samples.

Amino Acid Sequence↗

PubMed1997

Lead modulation of the neuronal nicotinic acetylcholine receptor in PC12 cells.

Lead is known to modulate several ligand- and voltage-gated ion channels, including the nicotinic acetylcholine receptor (AChR) channel. We examined the effects of lead on the nicotinic AChR in rat clonal phaeochromocytoma PC12 cells using whole-cell and single-channel patch-clamp techniques to clarify the detailed mechanism of action. Lead suppressed acetylcholine-induced currents in a dose-dependent manner with an EC50 value of 37 microM and a Hill coefficient of 0.82. At the single-channel level, 1-10 microM lead shortened the opening and burst durations, and increased the duration of mean closed time. The open probability was significantly decreased by lead. These changes of single-channel kinetics result in a significant decrease in the total charge carried through the open AChR channels explaining the suppressive effect of lead on acetylcholine-induced whole-cell currents.

Acetylcholine↗

PubMed1997

Monocarboxylic acids enhance the anesthetic action of procaine by decreasing intracellular pH.

Sodium monocarboxylates are known to enhance the anesthetic action of procaine, and also decrease intracellular pH (pHi). We studied the effect of 30 mM Na monocarboxylates (formate, acetate, propionate, butyrate, and salicylate) on the pHi and on the anesthetic action of procaine HCl using giant axons of crayfish (Procambarus clarkii). The pHi was measured using pH sensitive microelectrode method and the anesthetic action was evaluated by the change in the action potential (AP) amplitude. The tested acids except for formate showed apparent decrease in pHi and enhancement of the action of 2 mM procaine. Other organic acids (maleate and benzensulfonate) did not affect pHi and anesthetic action of procaine. In the bicarbonate free solution, pHi increased and the anesthetic action was weakened. The EC25 values (the concentration of procaine which depresses the AP amplitude by 25%) of acetate, propionate, and bicarbonate free solution were coincided with the predicted EC25 values from the simple simulation on intracellular procaine increase according to the pHi change. But the EC25 value of salicylate group was less than half of the predicted. These results suggested that the enhancing action of straight chain monocarboxylic acids is due to pHi decrease, and salicylate has other additional mechanisms.

Action Potentials↗

PubMed1997

Effect of long-term exogenous hyperinsulinemia and fructose or glucose supplementation on triglyceride turnover in rats.

We examined the effect of long-term (6 months) hyperinsulinemia on VLDL-triglyceride turnover in male Wistar rats. Hyperinsulinemia was induced in rats by daily s.c. injection of Ultralente insulin (6 U/day at 19:00). Fructose (F) or glucose (G) was supplied in the drinking water (10%) in order to prevent hypoglycemia. The rats were divided into 5 groups: (1) hyperinsulinemia with F water: group F + I; (2) hyperinsulinemia with G water: group G + I; (3) F water alone: group F; (4) G water alone: group G; and (5) control rats without sugar water group C. After 6 months of daily insulin injection triglyceride secretion rate (TGSR) was estimated using Triton WR1339 in all the rats. Groups F + I and G + I were obese and hypoglycemic compared to the other groups. Fasting plasma glucose level of group F was higher than any other group value. TGSR of group F + I was significantly higher than that of the control group, while that of group G + I was not, indicating that long-term hyperinsulinemia can stimulate hepatic triglyceride production when the rats were supplemented only with fructose. On the other hand, the rats in group G + I showed the lowest plasma free fatty acid level of all and their postheparin lipolytic activity was significantly elevated compared to that of the control rats. Moreover, they had suppressed plasma triglyceride levels and its fractional catabolic rate was significantly increased, suggesting that hyperinsulinemia can still stimulate triglyceride removal from the circulation of glucose supplemented rats even at month 6. In conclusion, exogenous hyperinsulinemia can stimulate hepatic triglyceride secretion even after 6 months duration when supplemented with fructose, while its stimulating effect on triglyceride removal from the circulation can be seen only with glucose supplementation. Thus, the effect of long-term hyperinsulinemia on plasma triglyceride turnover differs depending on the supplemented monosaccharides.

Animals↗

PubMed1997

A specific loss of growth hormone abolished sex-dependent expression of hepatic cytochrome P450 in dwarf rats: reversal of the profiles by growth hormone-treatment.

A spontaneous dwarf rat derived from a colony of Sprague-Dawley (SD) strain has no detectable level of growth hormone (GH) in pituitary, although it contained other hormones like prolactin and ACTH. Hepatic profile of cytochrome P450 (P450) differed clearly between dwarf and normal SD rats. A male-specific form of P450, CYP2C11, was detected in dwarf male rat livers, while the level was one-third of the normal SD livers. This P450 was also detected in dwarf females. Other male-specific CYP3A2 and CYP3A18 were also contained in both sexes of dwarf rats, whereas a female-specific form, CYP2C12, was not detectable in dwarf females. Phenobarbital-inducible CYP2B1 and CYP2B2 were constitutively expressed in dwarf rats, although substantially absent in normal SD rats. To assess the role of GH on hepatic P450 expression, GH was given to dwarf rats for 7 to 9 days. The intermittent injection (mimicking the male secretory pattern) resulted in the elevation of CYP2C11 to a level as observed in normal SD males. Continuous infusion of GH (mimicking the female secretory pattern) evoked CYP2C12 in livers of both sexes of dwarf rats, whereas the treatment decreased levels of CYP3A2, CYP3A18, and CYP2B1. These results clearly demonstrate that specific defect of GH, but not pituitary, cause the clear changes in hepatic P450 forms including sex-specific forms. The present study provides evidence further to strengthen the principal role of GH on the regulation of expression of P450 in rat livers.

Animals↗

PubMed1997

Tandem duplication of the MLL gene in myelodysplastic syndrome-derived overt leukemia with trisomy 11.

Trisomy 11 as a sole chromosomal abnormality is a rare aberration observed in myelodysplastic syndrome (MDS) or acute myeloblastic leukemia (AML). Recently a partial tandem duplication of the MLL gene, located on chromosome band 11q23, has been identified in de novo AML with trisomy 11. We describe a 72-year-old woman suffering from MDS-derived overt leukemia with trisomy 11 and a tandem duplication of the MLL gene. At first the patient was found to have myeloblasts with Auer rods in the peripheral blood and diagnosed as MDS, refractory anemia with excess of blasts in transformation (RAEB-T). After 2 months a picture of overt leukemia (AML; M2) developed as shown by an increased number of myeloblasts. Various chemotherapy regimens had little effect, and she died of disease progression 15 months after admission. During her clinical course, the chromosome analyses consistently showed 47,XX, +11. Southern blot analysis of leukemic blasts on admission and in accelerated phase revealed identical rearranged bands of the MLL gene. Fluorescence in situ hybridization analysis excluded the possibility of masked translocation of the MLL gene to other chromosomes. Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis using a forward exon 6 primer and a backward exon 3 primer demonstrated an in-frame fusion of exon 8 with exon 2. Our results indicated that a partial tandem duplication of exons 2-8 of the MLL gene could be observed in MDS-derived overt leukemia as well as de novo AML with trisomy 11.

Aged↗

PubMed1997

High prevalence of GAD65 (and IA-2) antibodies in Japanese IDDM patients by a new immunoprecipitation assay based on recombinant human GAD65.

Marked differences have been reported in the prevalence of glutamic acid decarboxylase (GAD) antibodies between Caucasian (63-84%) and Japanese (30-50%) or Asian (5-50%) IDDM patients. Using a new immunoprecipitation assay based on 125I-labelled recombinant human GAD65 we have reassessed prevalence of GAD65 antibodies in Japanese patients. We also assessed prevalence of IA-2 antibodies. GAD65 antibodies were detected in 83.3% of sera taken within 1 year of onset, comparable to the prevalence reported in Caucasian patients. Positivity decreased to 66.7% after 2 to 3 years and to 54.3% after 3 years from onset, still higher than previously reported Asian prevalence. Except in one patient, high antibody levels persisted chronically, up to 12 years. There was no difference in the prevalence of GAD65 antibodies between Japanese IDDM patients with and without autoimmune thyroid disease (AITD). IA-2 antibodies were detected in 64.7% of sera taken within 1 year of onset. Prevalence of IA-2 antibodies was lower than that of GAD65 antibodies. The difference in positivity in Asian IDDM patients between present and previous reports arose from the sensitivity of our assay for GAD65 antibodies. Additionally, the patients we studied had classic IDDM with a well-defined onset. We conclude that prevalence of GAD65 antibodies in Japanese IDDM patients is comparable to that in Western studies. There was no relationship of GAD65 antibody positivity to coexistence of AITD. Our results suggest that autoimmunity is the most significant cause of Japanese IDDM.

Adolescent↗

PubMed1997

Induction of heat shock protein 72 synthesis by endogenous tumor necrosis factor via enhancement of the heat shock element-binding activity of heat shock factor 1.

Endogenous tumor necrosis factor (enTNF) acts as a resistance factor against cytotoxicity caused by heat by inducing manganous superoxide dismutase (MnSOD), thereby scavenging reactive oxygen free radicals. On the other hand, it is also well known that heat shock proteins (HSP) which are induced by heat stress behave as cytoprotective factor against this stress. However, the relationship of these two resistance factors is not elucidated yet. In the present study, we therefore proposed the possibility that enTNF enhances HSP72 expression. Heat-sensitive L-M (mouse tumorigenic fibroblast) cells, which normally do not express enTNF, were transfected with a nonsecretory-type human TNF-alpha expression vector to produce enTNF. Stable transfectants showed resistance to heat treatment and an increase of HSP72 expression. Conversely, when HeLa (human uterine cervical cancer) cells, which normally produce an appreciable amount of enTNF, were transfected with an antisense TNF-alpha mRNA expression vector to inhibit enTNF synthesis, their heat sensitivity was enhanced and HSP72 expression was reduced by half. Although enTNF caused no difference in the level of heat shock factor (HSF) 1 in these cells, enTNF expression correlated well with the binding activity of HSF-1 to a 32P-labeled synthetic oligonucleotide containing the human heat shock element (HSE). These results indicate that enTNF participates not only in intrinsic resistance against heat via induction of MnSOD but also via enhancement of the HSE-binding activity of HSF 1 followed by augmentation of HSP72 expression.

Animals↗

PubMed1997

Heat shock and the role of the HSPs during neural plate induction in early mammalian CNS and brain development.

We have investigated the early development expressional of the heat shock protein genes (hsps) and HSP synthesis and their role during neuroectoderm induction, differentiation and early CNS formation. The expression and kinetics of 90, 73/71, 47 and 27 HSPs on neuroectoderm differentiation was compared under normal and stressed conditions. The role of HSPs on neuroctoderm cell fate including thermotolerance and apoptosis using a whole in vitro embryo culture system was studied. Hsp expression appears closely linked in early mammalian development to critical differentiation and proliferation stages in early brain and heart formation. The hsps are developmentally activated around blastula stage and HSPs are constitutively expressed at high levels during neural tube closure and are heat shock responsive. Using both Northern analysis, confocal microscopy and whole mount in situ hybridisation we have identified the mRNA hsp transcripts and HSPs during organogenesis. HSPs were detected during neuroectoderm cell induction and differentiation with the hsp mRNA being tightly regulated during the cell cycle of neuroectoderm especially at early fore-, mid-, hindbrain and heart formation. The 'chaperone' functions of the HSPs are well known, recently during gastrulation the HSP47 and 27 have been shown to specifically bind and fold to nascent collagen and actin molecules respectively. This role is essential for the formation of the basement membrane, extra cellular matrix and neural crest migration during neural plate development. HSP function was observed by using anti-sense strategy, short '5 anti-sense cDNA' hsp oligonucleotides inhibited hsp expression during gastrulation in the whole embryo cultures. The developmental activation of the heat shock element (HSE) is essential to our understanding of the HSPs role in neuronal cell fate. Using specific polyclonal antibodies to HSF1 and 2 (Dr Nakai, Kyoto University) the expression of heat shock factors (HSFs) during neuroectoderm differentiation was examined. Using Western analysis, confocal microscopy and flow cytometry HSF1 and 2 were identified and studied under both normal and heat shocked conditions. During gastrulation higher levels of HSF1 and 2 were identified in the neuroectoderm layer especially in regions of the fore-, mid- and hindbrain. The heat shock response and activation of the HSPs 90, 70, 47 and 27 families have been correlated with HSF1 and 2. The HSF1 appears to be present in all early embryonic cells but appears not to bind to the HSE until early head fold stage at gastrulation when the presence of HSF2 is observed. During neuroectoderm differentiation the activation of HSF1 and 2 appears to correlate with high constitutive expression of many of the hsps specifically hsp90, 73, 71, 47 and 27 being tightly regulated by the cell cycle at neurulation.

Animals↗

PubMed1997

Regional correlations between the EEG and oxygen metabolism in dementia of Alzheimer's type.

To determine the relationship between EEG slowing and cerebral hypometabolism in dementia, 10 patients with dementia of Alzheimer's type (DAT) were evaluated with quantitative topographic EEG and positron emission tomography (PET). Power in each 1-Hz frequency band from 2-20 Hz, power ratio index, and normalised PET data from corresponding cortical sites were compared to data obtained from 20 normal volunteers. PET revealed significant parieto-temporal hypometabolism, and topographic EEG mapping and power spectrum analysis revealed a slowing of the background EEG that was most pronounced in the parietal-temporal areas. Correlation analysis between EEG power spectrum data and CMRO2 revealed significant negative correlations for frequencies below 8 Hz and significant positive correlations above 8 Hz in the parieto-temporal regions, which have previously been identified as the areas most severely affected by pathological changes associated with DAT. Correlation coefficients plotted as functions of frequency illustrated the relationships between EEG changes and reduced CMRO2, supporting previous views that EEG slowing in DAT may be related to hypometabolism in cortical regions most affected by the disease.

Aged↗

PubMed1997

S-8921, an ileal Na+/bile acid cotransporter inhibitor decreases serum cholesterol in hamsters.

The ileal Na+/bile acid cotransporter (IBAT) maintains the reabsorption of bile acids from the intestine in the enterohepatic circulation of bile acids. In the present study, we showed that S-8921 could dose-dependently inhibit the uptake of [3H] taurocholate in the COS7 cell line which constitutively expresses hamster IBAT. The IC50 value of S-8921 against 60 microM of [3H] taurocholate uptake was 66 +/- 8 microM and kinetic analysis revealed that the inhibition by 100 microM of S-8921 was a mixture of competitive and non-competitive types. In vivo administration of S-8921 by its incorporation into diet (0.001-0.1%) caused dose-dependent decrease of serum cholesterol concentrations accompanied by increased fecal excretion of bile acids in hamsters which were not loaded with cholesterol and bile acid. These data suggest that the inhibition of IBAT could decrease serum cholesterol in the non-cholesterol and -bile acid loaded normal condition.

Absorption↗

PubMed1997

MUC2 gene expression is found in noninvasive tumors but not in invasive tumors of the pancreas and liver: its close relationship with prognosis of the patients.

We have previously reported that MUC2 apomucin was highly expressed in noninvasive tumors of the pancreas (intraductal papillary tumor [IdPT]) and liver (bile duct cystadenocarcinoma [BdCC]), which show more favorable outcomes than invasive carcinomas. In contrast, MUC2 was rarely expressed in invasive carcinomas of the pancreas (invasive ductal carcinoma [IDC]) and the liver (invasive cholangiocarcinoma [ICC]). In the present study, we examined localization of MUC2 messenger RNA (MUC2 mRNA) by using a complementary DNA (cDNA) probe for the MUC2 tandem repeat for in situ hybridization (pHAM1). Localization of MUC2 apomucin was determined by using an antibody directed against MUC2 apomucin (anti-MRP) for immunohistochemistry study. Eleven IdPTs and 10 IDCs of the pancreas, and 8 BdCC and 8 ICCs of the liver were examined. Nine (82%) of 11 IdPTs showed positive expression of MUC2 mRNA in the neoplastic cells, whereas none (0%) of the IDCs showed expression of MUC2 mRNA. Six (75%) of the 8 BdCCs showed positive expression of MUC2 mRNA in the neoplastic cells, whereas none (0%) of the 8 ICCs showed expression of MUC2 mRNA. The localization of MUC2 mRNA and that of MUC2 apomucin usually coincided, although a few cases (1 IDC, 1 BdCC, and 1 ICC) showed focal expression of MUC2 apomucin despite the absence of detectable MUC2 mRNA. These results indicate that the expression of MUC2 apomucin in IdPTs and BdCCs correlates with expression of MUC2 mRNA. In both patient groups with pancreatic tumors and hepatic tumors, patients with positive MUC2 mRNA expression in the tumors showed significantly better survival than those with negative MUC2 mRNA expression in the tumors. The production of MUC2, an abundant extracellular mucin, by most IdPTs and BdCCs may be correlated with tumors that display lower levels of invasion and metastasis.

Aged↗

PubMed1997

Increased theophylline metabolism in the menstrual phase of healthy women.

BACKGROUND: We previously reported on a Japanese woman with premenstrual asthma whose serum theophylline concentration was lower before the onset of her menstrual period. We evaluated the clearance of theophylline in each phase of her menstrual cycle and found an increase in clearance in the premenstrual and menstrual phases. OBJECTIVE: This study was designed to investigate whether changes in theophylline clearance may occur with the menstrual cycle in nonasthmatic women. METHODS: Aminophylline, 250 mg, was infused intravenously for 45 minutes, and the clearance of theophylline was calculated in seven healthy, ovulatory women on days 1 or 2, 10, and 20 or 25 of the menstrual cycle. The serum concentration of theophylline was determined with an enzyme immunoassay (homogeneous). RESULTS: Theophylline clearance was significantly higher and its half-life was significantly shorter in the menstrual phase than in the follicular phase. CONCLUSION: The metabolism of theophylline, and consequently, its clearance were increased in healthy women around the onset of menses. Clinicians must therefore consider the menstrual variation in theophylline metabolism when prescribing this drug to female patients.

Adult↗

PubMed1997

Bombyxin, an insulin-related peptide of insects, reduces the major storage carbohydrates in the silkworm Bombyx mori.

The effects of an insect insulin-related peptide, bombyxin, on carbohydrate metabolism were investigated in the silkworm Bombyx mori. Bombyxin lowered the concentration of the major hemolymph sugar, trehalose, in a dose-dependent manner when injected into neck-ligated larvae. Bombyxin also caused elevated trehalase activity in the midgut and muscle, suggesting that bombyxin induces hypotrehalosemia by promoting the hydrolysis of hemolymph trehalose to glucose and thereby facilitating its transport into tissues. In addition, bombyxin reduced the glycogen content in the fat body and concurrently raised the percentage of active glycogen phosphorylase in this tissue. Because hemolymph trehalose is also a major storage form of carbohydrate in insects, our results indicate that bombyxin reduces the amount of both principal storage carbohydrates in B. mori larvae. It is therefore suggested that although bombyxin is involved in the control of carbohydrate metabolism like insulin, the physiological role of bombyxin in insects is different from that of insulin in mammals.

Animals↗