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Biomedical subjects

M Tsutsui

Publications and source records attributed to M Tsutsui.

At least 73 records · Page 4Linked to original sources
PubMed1994

Three types of "mid-band" lipoproteins in non-insulin-dependent diabetes mellitus: relation to metabolic abnormalities and vascular complications.

A number of fine bands which occur in positions between the beta- and pre-beta-lipoproteins in polyacrylamide gell electrophresis are called mid-bands (MB). In this study, the relationship between the occurrence of these MB and metabolic abnormalities or vascular complications was evaluated in 181 patients with non-insulin-dependent diabetes mellitus (NIDDM). The incidence of MB in diabetic patients was significantly higher than that in 149 healthy control subjects (35 vs. 20%, p < 0.01). Analysis according to the type of MB revealed that the incidence of the central type in diabetic patients was significantly higher than that in healthy control subject (11 vs. 5%, p < 0.05). When the values of HbAlc were elevated, the incidence of MB and its central type slightly increased. The occurrence of the lower type of MB showed no relationship with the levels of HbAlc. The incidence of MB and its central type were significantly higher in patients with type IIb hyperlipidemia (86 and 41%, respectively) and with type IV hyperlipidemia (63 and 25%) than in those with normolipidemia (21 and 5%) (p < 0.01 of all). The incidence of the lower type of MB was significantly higher in patients with type IIa hyperlipidemia (25%) and with type IIb hyperlipidemia (36%) than in those with normolipidemia (11%) (p < 0.05, p < 0.01, respectively). There was no significant difference in the occurrences of MB and of the central and lower types of MB between the normolipidemic patients and healthy control subjects. The incidence of MB and its central type were significantly higher in patients with nephropathy (54 and 23%, respectively) than in those without nephropathy (32 and 9%) (p < 0.05 of all). There was no significant difference in the incidence of lower type of MB between patients with and without nephropathy. These results indicate that the incidence of central type of MB may be high in NIDDM, and that the occurrence of central type may be associated with abnormal metabolism of glucose or lipid and with diabetic nephropathy.

Aged↗
PubMed1994

Different change in lipoprotein(a) levels from lipid levels of other lipoproteins with improved glycemic control in patients with NIDDM.

OBJECTIVE: To evaluate change both in lipoprotein(a) [Lp(a)] and lipid levels in other lipoproteins in non-insulin-dependent diabetes mellitus (NIDDM) after short-term improvement of glycemic control. RESEARCH DESIGN AND METHODS: We compared Lp(a) levels in 210 NIDDM patients with those in 46 control subjects and evaluated the relationship between glycemic control and Lp(a) levels in diabetic patients. In addition, changes in Lp(a) levels and lipid levels were assessed after the improvement of glycemic control in 54 poorly controlled NIDDM patients. RESULTS: In NIDDM, Lp(a) levels in all patients, 62 patients with HbA1c < 6.0%, and 75 patients with HbA1c between 6.0 and 8.0%, were significantly higher than those in control subjects (19.1 [1.7-106.6], 19.2 [6.0-106.6], and 20.3 [2.7-75.3] vs. 15.4 [2.0-61.7] mg/dl, median [range], P < 0.05). Lp(a) levels in 73 patients with HbA1c of > or = 8.0% (18.7 [1.7-58.8] mg/dl) were not significantly different from those in control subjects. After glycemic control, lipid levels in plasma and in other lipoproteins fell significantly, but Lp(a) did not change (from 18.3 [1.7-58.8] to 18.4 [6.6-95.3] mg/dl). Changes in lipid levels, including Lp(a), did not correlate with those in fasting plasma glucose or HbA1c. CONCLUSIONS: These results suggest that elevated Lp(a) levels do not reflect poor glycemic control and that Lp(a) levels are independent of lipid levels in other lipoproteins after improved glycemic control in NIDDM.

Blood Glucose↗
PubMed1994

Stimulatory guanine nucleotide binding protein in pig epidermis: transient increase of the 45KDA cholera toxin substrate (Gs alpha) in the tape stripping-induced hyperproliferative state.

Cholera toxin catalyzed the transfer of ADP-ribose from [alpha-32P] NAD to 45kDa protein in pig epidermis. Western blot analysis using anti-Gs alpha antibody identified the 45kDa protein to be Gs alpha. In contrast to pertussis toxin-catalyzed ADP-ribosylation of Gi alpha, the cholera toxin-catalyzed ADP-ribosylation was enhanced by the presence of Mg2+ in the reaction mixture. The cholera toxin-catalyzed ADP-ribosylation of the epidermal 45kDa membrane protein was significantly decreased, when samples were prepared from the cholera toxin-pretreated epidermis. The results, coupled with our previous report (Tsutsui and Iizuka 1990), indicate that pig epidermis contains functional G proteins (Gs and Gi), that affect the epidermal adenylate cyclase activity. Tape stripping-induced hyperproliferative epidermis showed an increased cholera toxin-catalyzed ADP-ribosylation of the 45kDa protein (Gs alpha) at 12-24 h following the tape stripping. Immunoblot analysis, however, showed no remarkable change in the level of Gs alpha compared with non-stripping controls. There was no significant difference in the level of the pertussis toxin-induced ADP-ribosylation of 40kDa protein (Gi alpha) in the tape-stripped epidermis. Immunoblot analysis showed no change in Gi content, either. Forskolin-induced cyclic AMP accumulation was markedly increased in the tape stripping-induced hyperproliferative epidermis. Cholera toxin-induced cyclic AMP accumulation was slightly increased, but this was not statistically significant. These results indicate that the alteration of Gs that is documented by cholera toxin-catalyzed ADP-ribosylation, is among the functional derangements of adenylate cyclase of tape stripping-induced hyperproliferative epidermis.

Adenosine Diphosphate Ribose↗
PubMed1994

Correlation of activation of Ca2+/calmodulin-dependent protein kinase II with catecholamine secretion and tyrosine hydroxylase activation in cultured bovine adrenal medullary cells.

We have investigated the activation of Ca2+/calmodulin-dependent protein kinase II (CaM kinase II) in cultured bovine adrenal medullary cells. The activation was assayed as an increase in the Ca(2+)-independent (autonomous) activity of CaM kinase II, using the synthetic substrate Syntide-2. Incubation of cells with acetylcholine increased the Ca(2+)-independent activity in a time (20 sec to 5.0 min)- and concentration (10-300 microM)-dependent manner. These curves were closely correlated with those of catecholamine secretion and tyrosine hydroxylase activation. Removal of extracellular Ca2+ completely abolished the stimulatory effects of acetylcholine on the Ca(2+)-independent activity, as well as on catecholamine secretion and activation of tyrosine hydroxylase. Nicotine but not muscarine increased the Ca(2+)-independent activity as potently as did acetylcholine, and hexamethonium but not atropine completely blocked the acetylcholine-induced increase. In 32P-labeled cells, acetylcholine stimulated the phosphorylation of a 50-kDa protein that was immunoprecipitated with an anti-brain CaM kinase II antibody. These results suggest that acetylcholine stimulates CaM kinase II activity through nicotinic acetylcholine receptor-mediated influx of Ca2+ and that the activation of CaM kinase II is closely related to catecholamine secretion and tyrosine hydroxylase activation in cultured adrenal medullary cells.

Acetylcholine↗
PubMed1994

C-type natriuretic peptide stimulates catecholamine synthesis through the accumulation of cyclic GMP in cultured bovine adrenal medullary cells.

We examined the effects of C-type natriuretic peptide (CNP) on cyclic GMP production and catecholamine synthesis in cultured bovine adrenal medullary cells. 1) CNP increased intracellular cyclic GMP content in a concentration-dependent manner (10-1000 nM). 2) The cyclic GMP production induced by 1 microM CNP reached a 200-fold increase, and the effect of CNP was most potent among the natriuretic peptide family. 3) The CNP-induced cyclic GMP production was attenuated by endothelin (1 microM) and angiotensin II (0.1-1 microM). 4) When the cells were cultured with hypertonic NaCl medium, the CNP-induced cyclic GMP production was potentiated in a time (1-4 days)- and concentration (25-100 mM)-dependent manner. 5) CNP stimulated the synthesis of 14C-labeled catecholamines from [14C] tyrosine but not from [14C] dopa. The stimulatory effect of CNP on the 14C-labeled catecholamine synthesis was observed at the concentrations of 100 to 100 nM. 6) 8-Bromo cyclic GMP, a membrane-permeable cyclic GMP analog, and sodium nitroprusside, an activator of soluble guanylate cyclase, also stimulated the synthesis of 14C-labeled catecholamines from [14C]tyrosine, whereas C-ANF, a specific ligand for the ANP-C (clearance) receptor that does not increase cyclic GMP content, failed to stimulate the synthesis of 14C-labeled catecholamines. 7) CNP (1 microM) as well as 8-bromo cyclic GMP and sodium nitroprusside increased the activity of tyrosine hydroxylase in the cells. These results suggest that in the adrenal medulla, CNP is a potent agonist for cyclic GMP production, which is modulated by endothelin, angiotensin II and the hypertonic NaCl condition.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Medulla↗
PubMed1994

Occurrence and activation of Ca2+/calmodulin-dependent protein kinase II and its endogenous substrates in bovine adrenal medullary cells.

We investigated the presence of and the endogenous substrates for Ca2+/calmodulin-dependent protein kinase II (CaM kinase II) in cultured bovine adrenal medullary cells. By a series of chromatographic steps using DEAE-cellulose, calmodulin affinity, and Sephacryl S-300 columns, we partially purified two CaM kinases (peaks I and III) and one calmodulin-binding protein (peak II). Both of the kinases (peaks I and III) showed broad substrate specificities. Peak I, but not peak III, was immunoprecipitated with an antibody against rat brain CaM kinase II, suggesting that peak I is CaM kinase II or a closely associated CaM kinase. Although the anticaldesmon antibody recognized a 77-kDa protein (low molecular mass caldesmon) in crude preparations from the cells, the protein in peak II was not immunoblotted with the antibody. The peak II protein was phosphorylated by the CaM kinase in peak I but not by the CaM kinase in peak III. Peak I kinase also phosphorylated purified tyrosine hydroxylase and several proteins from chromaffin granule membranes. Stimulation of cultured bovine adrenal medullary cells with 56 mM K+ evoked rapid increases in 45Ca2+ influx and autonomous CaM kinase II activity, both of which were attenuated by the addition of 20 mM MgSO4, an inhibitor of voltage-dependent Ca2+ channels. These results suggest that an isozyme of CaM kinase II exists in adrenal medullary cells and is activated by cell depolarization. Furthermore, the peak II protein is apparently a novel endogenous substrate for CaM kinase II.

Adrenal Medulla↗
PubMed1993

Receptors for C-type natriuretic peptide in cultured rat glial cells.

To characterize sites of action of C-type natriuretic peptide (CNP) in the glial cells, the effect of CNP on cGMP accumulation and the binding of [125I]CNP in rat astrocyte RCR-1 cells were studied. CNP stimulated cGMP accumulation in the cells from 10(-9) M in a dose-dependent manner, but ANP (atrial natriuretic peptide) had a negligible effect on cGMP accumulation in the cells. [125I]CNP was bound to the cells and its Kd value was 2 orders of magnitude lower than that of the ED50 value for stimulation of cGMP accumulation in the cells. Not only CNP but also ANP displaced [125I]CNP binding to the cells. These results suggest that RCR-1 cells have a B-receptor which contains a guanylate cyclase domain and is preferentially activated by CNP, and that they also have a C-receptor which does not contain a guanylate cyclase domain that reacts with both ANP and CNP.

Animals↗
PubMed1993

Mutagenicity of blue rayon extracts of human bile in the Ames test.

The mutagenicity of human bile was examined in the Ames Salmonella/microsome assay. Bile samples were obtained from the gallbladders resected from patients with cholelithiasis, choledocholithiasis, gallbladder cancer, extrahepatic bile duct cancer and other diseases. For extraction of mutagenic components, the bile samples were treated with blue rayon and the adsorbed materials were assayed with Salmonella typhimurium TA98 in the presence of S9 mix. Twenty-four bile samples were tested and positive mutagenic activity was found in 14 samples. A 200-microliter bile equivalent material gave 6.3 times as many revertant colonies as the solvent control. With several samples that had undergone two cycles of blue rayon extraction, clear dose-response relationships in mutagenicity were demonstrated.

Adult↗
PubMed1993

Intracellular magnesium deficiency in acute myocardial infarction.

It has been hypothesized that intracellular magnesium deficiency is a pathogenetic factor in acute myocardial infarction. This study examined the time course of changes in the erythrocyte magnesium concentration and the correlation between the erythrocyte magnesium concentration and the severity of acute myocardial infarction in 49 consecutive patients with transmural acute myocardial infarction. The data were compared with results from 20 control patients without ischemic heart disease. The erythrocyte magnesium concentration (mg/dl) decreased significantly during the acute phase of the infarction (4.86 +/- 0.09 on day 1, 4.89 +/- 0.10 on day 2 and 4.86 +/- 0.10 on day 3 versus 5.26 +/- 0.19 for controls, all P < 0.05) and then normalized gradually to 5.25 +/- 0.10 on day 28. The serum magnesium concentration (mg/dl) also decreased significantly during the acute phase of the infarction (1.93 +/- 0.04 on day 1 and 2.11 +/- 0.03 on day 2 versus 2.26 +/- 0.08 for controls, all P < 0.05), before recovering to 2.28 +/- 0.06 on day 28. There were significant correlations between the erythrocyte magnesium concentration on day 1 and maximal values of serum cardiac enzymes (r = -0.30 for creatine kinase, r = -0.34 for glutamic oxaloacetic transaminase and r = -0.57 for lactate dehydrogenase, all P < 0.05). Moreover, the erythrocyte magnesium concentration was significantly lower in patients with (4.32 +/- 0.08 mg/dl, n = 13) than in those without (5.06 +/- 0.09 mg/dl, n = 36, P < 0.0001) serious arrhythmias. These data indicate that intracellular magnesium deficiency is involved in the acute phase of myocardial infarction.

Adult↗
PubMed1992

Acid cholesteryl ester hydrolase activity of mononuclear leukocytes in patients with non-insulin-dependent diabetes mellitus: studies before and after treatment of diabetes.

The change of acid cholesteryl ester hydrolase activity in mononuclear leukocyte following treatment of diabetes mellitus was studied in 21 patients with non-insulin-dependent diabetes mellitus (NIDDM). Enzyme activity before treatment in the patients was significantly lower than that in 14 age-matched healthy subjects (1.20 +/- 0.15; mean +/- S.E. vs. 2.20 +/- 0.17 nmol/mg protein/h, P less than 0.01). Enzyme activity before treatment in the patients was significantly increased (P less than 0.05) after 4-8 weeks of treatment. However, enzyme activity of 1.43 +/- 0.14 nmol/mg protein/h observed after treatment in the patients was significantly lower (P less than 0.01) than that in the healthy subjects. There was a significant negative correlation between enzyme activity before treatment and the increase in enzyme activity following treatment (rs = -0.555, P less than 0.01, n = 21). These results indicate that low level of enzyme activity may be insufficiently improved by the treatment of diabetes, and the risk for the development of atherosclerosis as viewed from the enzyme activity may persist even after the treatment in NIDDM.

Adult↗
PubMed1992

Flow cytometric analysis of pig epidermal keratinocytes: effects of tape stripping.

Tape stripping is a dynamic in vivo model for the induction of synchronized keratinocyte proliferation. We investigated the cell kinetics of pig epidermis by DNA-flow cytometric analysis, which was compared with [3H]thymidine incorporation mitotic counts and 2-[3H]-deoxy-D-glucose uptake. The stripping was standardized and confirmed histologically by the observation of complete removal of horny layer. Following the stripping, the proportion of cells in S-phase showed no remarkable change until 12 h. This was followed by a spike-like increase in the S-phase cells, the peak of which was reached at 24 h. This gradually decreased and returned to basal levels by 48 h. The cells in G2/M fraction initially decreased; the lowest value was obtained at 12 h. This was followed by a marked increase in the G2/M fraction, the peak of which was at 36 h. The keratinocytes in G2/M fraction gradually returned to basal levels by 96 h. [3H]Thymidine uptake and mitotic counts were mostly parallel with the data of the flow cytometric analysis, suggesting the latter as being a reliable system for cell kinetic analysis. The glucose uptake initially decreased (at 6 h following the stripping) and then increased at 24 h. Histologically the stripped epidermis regained its horny layer almost completely by 72 h following the stripping; this was occasionally accompanied by a moderate acanthotic change thereafter.

Animals↗
PubMed1992

Alcohol-induced sinus bradycardia and hypotension in patients with syncope.

We observed 2 cases of repeated episodes of syncope after alcohol ingestion. Both patients were light drinkers and had carotid sinus hypersensitivity. In both cases, alcohol loading tests repeatedly induced sinus bradycardia and hypotension 1.0-1.5 hours after drinking alcohol. Atropine was effective in improving symptoms. A loading test using a glucose solution of equivalent osmolarity and volume was negative. Acute alcohol ingestion usually increases heart rate with variable effects on blood pressure. However, our 2 cases exhibited unusual alcohol-induced sinus bradycardia and hypotension, suggesting a paradoxical increase in parasympathetic activity and/or decrease in sympathetic activity.

Aged↗
PubMed1991

Desensitization of the epidermal adenylate cyclase system: agonists and phorbol esters desensitize by independent mechanisms.

Exposure of pig epidermis to adenylate cyclase stimulators results in receptor-specific desensitization. We investigated the nature of the agonist-induced desensitization, which was compared with the phorbol ester-induced, receptor-nonspecific desensitization. Both phorbol ester-induced desensitization and the agonist-induced desensitization were accompanied by an increase in forskolin- and cholera toxin-induced cyclic AMP accumulations. The magnitude of the increase in the agonist-induced desensitization was parallel to the degree of the initial cyclic AMP accumulation; histamine and adenosine, which increase more cyclic AMP than epinephrine, resulted in a more marked increase in forskolin- and cholera toxin-induced cyclic AMP accumulations. Similarly, epidermis desensitized to multiple receptors revealed more marked forskolin- and cholera toxin-induced cyclic AMP accumulations than epidermis desensitized to a single receptor. In contrast to the phorbol ester-induced desensitization, agonist-induced desensitization was not affected by the protein kinase C inhibitors H-7 and staurosporin. Further, agonist-induced desensitization was still inducible in phorbol ester-desensitized epidermis and vice versa. In contrast to the agonist-induced desensitization, which is accompanied by the preceding adenylate cyclase stimulation, no evidence for the stimulation of the adenylate cyclase during phorbol ester treatment was obtained. Neither agonist-induced desensitization nor phorbol ester-induced desensitization affected the content of inhibitory guanine nucleotide binding protein of the epidermis, which was monitored by the pertussis toxin (IAP)-catalyzed ADP ribosylation reaction. Our results indicate that agonist-induced desensitization and the phorbol ester-induced desensitization are independent of each other. Although both processes are characterized by increased forskolin- and toxin-induced cyclic AMP accumulations, the former is accompanied by initial cyclic AMP accumulation; the latter is not.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1991

Transformation of arylamines into direct-acting mutagens by reaction with nitrite.

Arylamines including aniline (I), 1-naphthylamine (II), 2-naphthylamine (III), 2-aminofluorene (IV), 1-aminoanthracene (V) and 1-aminopyrene (VI) were treated with 4 equivalent amounts of nitrite at pH3 and 37 degrees C for 4 h. The reaction mixtures of I, IV, V and VI showed mutagenicity to Salmonella typhimurium TA98 and TA100 strains without metabolic activation. The numbers of His+ revertant colonies to TA98 strain were 110/0.05 mumole I, 970/0.055 mumole IV, 620/0.10 mumole V and 870/0.02 mumole VI. These arylamines were converted into mutagens with diazoquinone, diazonium and nitro functions depending on their structures. The mutagen from I was p-diazoquinone (I2). The mutagen from IV was highly unstable fluorene-2-diazonium salt (IV1). The mutagens from V were N3O3-introduced anthracene (V1-1) and 1-nitroanthracene (V2), and those from VI were unidentified nitro-introduced compound (VI1) and 1-nitropyrene (VI2).

1-Naphthylamine↗
PubMed1990

Inhibitory guanine nucleotide binding protein in pig epidermis: regulation of epidermal adenylate cyclase.

Islet-activating protein (IAP), one of the pertussis toxins, serving [alpha-32P]nicotinamide adenine dinucleotide (NAD) as a substrate for ADP ribosylation, radiolabelled a specific pig epidermal membrane protein. The IAP-specific substrate was detectable by sodium dodecyl sulphate-polyacrylamide gel electrophoresis as a single band corresponding to a molecular weight of 40 kDa. The ADP ribosylation catalysed by IAP was inhibited by the addition of Mg2+ to the reaction mixture. IAP is known to work on intact cell systems resulting in the ADP ribosylation using intracellular NAD as the ADP ribose donor. Following IAP pretreatment of intact pig epidermis, the epidermal receptor adenylate cyclase responses were markedly increased; all the stimulatory receptor adenylate cyclase responses (beta-adrenergic, prostaglandin E, adenosine and histamine responses) were significantly increased. Cholera toxin-induced cyclic AMP accumulation was also significantly increased. Forskolin-induced cyclic AMP accumulation was slightly increased after IAP pretreatment, but this was not statistically significant. The IAP-dependent ADP ribosylation of the epidermal 40 kDa membrane protein, which was prepared from the IAP pretreated epidermis, was significantly decreased. It is known that the tumour promoter, phorbol 12-myristate,13-acetate (PMA), decreases stimulatory receptor adenylate cyclase responses of the epidermis. Following the PMA pretreatment, IAP-dependent ADP ribosylation of the epidermal membrane protein was unaffected. Furthermore, following the PMA pretreatment, the IAP-induced increase in the epidermal receptor adenylate cyclase responses still remained. Our results indicate that pig epidermis contains 40 kDa membrane substrate for IAP-dependent ADP ribosylation, which has an inhibitory tonus on the epidermal adenylate cyclase until its ADP ribosylation by IAP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗
PubMed1990

Adenylate cyclase system in fetal rat keratinizing epidermal cells (FRSK cells) and SV40-transformed human keratinocytes.

The adenylate cyclase system of FRSK cells, a cultured cell line of fetal rat epidermal keratinocytes, and SV40-transformed human keratinocytes was investigated. Stimulators of the human epidermal adenylate cyclase, epinephrine, adenosine, and prostaglandin E2 increased cyclic AMP levels of these cells. There were marked differences in the stimulatory effects; while epinephrine revealed a much stronger effect than the other stimulators in FRSK cells, epinephrine and prostaglandin E2 revealed similarly marked effects in SV40-transformed cells. Histamine had little or only slight effect on the cyclic AMP levels of these cells. Cholera toxin and forskolin, which work on the stimulatory guanine nucleotide binding protein (Gs) and the catalytic component of adenylate cyclase, respectively, also increased cyclic AMP levels. Northern blot hybridization analysis revealed that both FRSK cells and SV40-transformed human keratinocytes express mRNAs for the beta 2-adrenergic receptor, as well as the stimulatory and inhibitory guanine nucleotide binding proteins (Gs and Gi, respectively). The presence of Gs as well as Gi were confirmed by cholera toxin-, and pertussis toxin (IAP)-induced ADP-ribosylation of membranous proteins of these cells. Our results indicate that both FRSK cells and SV40-transformed human keratinocytes express the fundamental components of the adenylate cyclase system. These cell lines might be useful tools for the analysis of the adenylate cyclase system in epidermal keratinocytes.

Adenosine↗
PubMed1990

Acid cholesteryl ester hydrolase activity of mononuclear leukocyte in type 2 (non-insulin-dependent) diabetic patients.

Acid cholesteryl ester hydrolase activity of mononuclear leukocytes was measured in 52 Type 2 (non-insulin-dependent) diabetic patients. Enzyme activity was significantly lower in the diabetic patients than in 14 age-matched control subjects (0.89 +/- 0.08 (mean +/- S.E.) vs. 2.20 +/- 0.17 nmol/mg protein/hr, p less than 0.01). In diabetic patients undergoing diet treatment only, the enzyme activity was significantly lower in poorly controlled patients than in well controlled patients (0.43 +/- 0.03 vs. 1.15 +/- 0.24 nmol/mg protein/hr, p less than 0.01). In the diabetic patients, there was a significant negative correlation between the enzyme activity and serum total cholesterol or low density lipoprotein cholesterol level (r = -0.361, p less than 0.01, n = 52 or r = -0.630, p less than 0.01, n = 28). These results suggest that a low level of acid cholesteryl ester hydrolase activity in mononuclear leukocyte might play an important role in the progression of atherosclerosis in Type 2 diabetes.

Carboxylic Ester Hydrolases↗