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PubMedDate not supplied

Comparison of the development of experimental pyelonephritis in homozygous brattleboro diabetes insipidus rats, heterozygous control rats and normal Wistar rats.

A comparative study was performed on haematogenous experimental pyelonephritis by injecting a Staphylococcus aureus suspension i.v. to homozygous and heterozygous Brattleboro and Wistar rats. The numbers of viable bacteria in blood, urine and kidney homogenates and the pathomorphological scores determined on the tenth day of infection were significantly lower in Brattleboro diabetes insipidus rats than in heterozygous Brattleboro and normal Wistar rats. The results suggest that homozygous Brattleboro rats are much more resistant to experimental pyelonephritis.

Animals↗
PubMed2004

An assay for determination of rat adrenal catechol-O-methyltransferase activity: comparison of spontaneously hypertensive rats and Wistar-Kyoto rats.

A method has been developed for measurement of catechol-O-methyltransferase (COMT) activity in the rat adrenal gland. Epinephrine, synthesized in the adrenal gland, was used as substrate, and its enzymatic product, metanephrine, was quantified by high-performance liquid chromatography (HPLC) with fluorescence detection. The method has sufficient precision and accuracy. Soluble (S) and membrane-bound (MB) COMT activity in Wistar-Kyoto (WKY) rats was 20.7 +/- 3.5 and 18.6 +/- 3.4 pmol min(-1) mg(-1) protein (n = 5), respectively. To clarify the role of adrenal COMT in blood-pressure regulation, S and MB COMT activity in spontaneously hypertensive rats were determined. Respective activity was 18.6 +/- 3.4 and 17.0 +/- 1.1 pmol min(-1) mg(-1) (n = 5), which is similar to that in WKY rats. This finding suggests that COMT in the adrenal gland might not be related to blood pressure regulation.

Adrenal Glands↗
PubMed1990

Genetically altered brain amino acid metabolism in spontaneously hypertensive rats: a study by using young spontaneously hypertensive rats and renal hypertensive rats.

Previously we demonstrated altered amino acid levels in brainstem regions of adult spontaneously hypertensive rats (SHR). For comparison, in this study, we determined amino acid concentrations in discrete brainstem regions in young prehypertensive SHR and renal hypertensive rats. In prehypertensive SHR, the content of glutamate was increased in the rostral ventrolateral medulla and the caudal ventrolateral medulla, and the content of beta-alanine was decreased in the nucleus tractus solitarii. In renal hypertensive rats, there was no change in glutamate and beta-alanine contents in all the regions. The profiles of contents of glutamate and beta-alanine in the brainstem regions in young SHR but not in renal hypertensive rats are the same as those found previously in adult SHR. Thus, the results of the present study suggest that the altered amino acid metabolism in the brainstem of SHR may be genetically inherent.

Amino Acids↗
PubMed1992

Human carcinoembryonic antigen cDNA expressed in rat carcinoma cells can function as target antigen for tumor localization of antibodies in nude rats and as rejection antigen in syngeneic rats.

We have tried to develop a new model consisting of rats transplanted with syngeneic colon carcinoma PROb cells transfected with cDNA coding for the carcinoembryonic antigen (CEA), the human tumor marker most commonly used as target for MAbs. The antigenic density of the 4 CEA-expressing clones selected for a precise characterization ranged from 5 x 10(4) to 1 x 10(6) CEA molecules per cell. In all clones the CEA was shown to be attached to the membrane by a phosphatidylinositol (PI) anchor. Using a panel of radiolabeled MAbs directed against the 5 major epitopes described on the CEA molecule, we showed that all these CEA epitopes were expressed by the 4 transfectants. Southern-blot analysis showed that the entire CEA cDNA was present in the transfectants. Western-blot analysis, however, showed that the size of the CEA expressed by the 4 transfectants was slightly smaller than that of CEA produced by 2 reference human colon-carcinoma cell lines. Two clones, expressing 1 x 10(5) and 1 x 10(6) CEA molecules per cell, respectively, were grafted s.c. in nude mice and rats. Injection of radiolabeled anti-CEA F(ab')2 fragments into these animals showed specific tumor localization with the highest percentages of injected doses for the transfectants expressing the highest CEA level. When grafted into immunocompetent syngeneic BDIX rats, the CEA-expressing clones induced a strong antibody response against CEA and tumor rejections in a majority of the animals. Although the analysis of the immune response against the CEA-cDNA-transfected carcinoma cells is under investigation, the present results demonstrate that human CEA could function as a rejection antigen when transfected into rat carcinoma cells.

Adenocarcinoma↗
PubMed1996

Effects of hysterectomy on bone in intact rats, ovariectomized rats, and ovariectomized rats treated with estrogen.

To determine whether the uterus plays any role in mediating the ability of estrogen to conserve bone in the rat, eight groups of animals (n = 8) with their skeletons labeled with 45Ca were studied. Rats were ovariectomized (OVX), hysterectomized (Hyst), or given sham operations (Sham) and then pair-fed a low-hydroxyproline casein diet for 4 weeks. The groups were treated orally with 17 beta-estradiol (E2) or vehicle, and serial measurements of biochemical markers of bone breakdown were made in weeks 1, 2, and 4. The femur density was measured by dual-energy X-ray absorptiometry (DXA), and skeletal calcium and 45Ca content were determined chemically. Final total body calcium values (mg) in the eight treatment groups were (means +/- SD): Sham, 2573 +/- 179; Sham + E2, 2635 +/- 159; Hyst, 2537 +/- 151; Hyst + E2, 2410 +/- 151; OVX, 2189 +/- 146; OVX + E2, 2559 +/- 172; OVX/Hyst, 2138 +/- 132; and OVX/Hyst + E2, 2460 +/- 140. Ovariectomy raised biochemical markers of bone resorption (urinary 45Ca, hydroxyproline, and deoxypyridinoline), lowered DXA bone mineral density, and reduced total body calcium and 45Ca content in both Hyst and Sham-Hyst animals (p < 0.001), whereas E2 treatment prevented these changes. Hysterectomy did not impair the ability of E2 to conserve bone in OVX rats. Thus, we conclude that estrogen-mediated induction of growth factors from uterine tissue does not play an essential role in mediating the bone-conserving actions of estrogen in the rat.

Animals↗
PubMed1982

The effect of ticlopidine on the aggregation of rat blood platelets and on the formation of metabolites from arachidonic acid and 8,11,14-eicosatrienoic acid in rat platelets during aggregation, and in the rat kidney.

The effect of ticlopidine after oral administration was determined on the aggregation of rat blood platelets and on the formation of cyclo-oxygenase, and lipoxygenase metabolites from arachidonic acid (AA) and 8,11,14-eicosatrienoic acid in rat platelets and in the kidney. 1. Platelet aggregation is inhibited by ticlopidine. The effect is dependent on the dose administered and the amount of collagen used to induce the aggregation. 2. After the incubation of platelets with [1-(14)C]AA and aggregation by collagen, the following substances are formed: thromboxane B2 (TxB2), 12L-hydroxy-5,8, 10-heptodecatrienoic acid (HHT), 12L-hydroxy-5,8,10,14-eicosatetraenoic acid (HETE) small amounts of PGE2 and PGD2 and an unknown metabolite. Ticlopidine administration during 3 days leads to an increase in the amounts of TxB2, PGE2, HHT and the unknown metabolite and a decrease in that of AA dependent on the dose administered. After 30 mg/kg the amount of HETE is decreased. 3. Under the same conditions, TxB1, PGE1, 12L-hydroxy-8,10-heptadecadienoic acid (HHD) and HETE (trienoic) are formed from [1-(14)C]8,11,14-eicosatrienoic acid. After 300 mg/kg ticlopidine the amounts of TxB1, PGE1 and HHD are increased. 4. In the rat kidney, [1-(14)C]AA is transformed into PGF 2 alpha, TxB2, PGE2, PGD2, PGA2, HHT and HETE. After ticlopidine administration, PGF 2 alpha, PGE2, PGD2 and PGA2 are increased, depending on the dose administered. 5. In this tissue, PGF 1 alpha, TxB1, PGD1, PGA1, HHD, HETE (trienoic) and an unknown metabolite are formed from [1-(14)C]eicosatrienoic acid. There is no effect from the administration of ticlopidine on the formation of these substances. 6. These results indicate that ticlopidine increases the synthesis of PGs and related substances in rat platelets and the kidney. This effect is due to an enhanced metabolism of AA.

8,11,14-Eicosatrienoic Acid↗
PubMed2002

Interactions of cationic drugs and cardiac glycosides at the hepatic uptake level: studies in the rat in vivo, isolated perfused rat liver, isolated rat hepatocytes and oocytes expressing oatp2.

This paper deals with a crucial mechanism for interaction of basic drugs and cardiac glycosides at the hepatic uptake level. Available literature data is provided and new material is presented to picture the differential transport inhibition of bulky (type2) cationic drugs by a number of cardiac glycosides in rat liver. It is shown that the so called organic anion transporting peptide 2 (oatp2) is the likely interaction site: differential inhibition patterns as observed in oocytes expressing oatp2, could be clearly identified also in isolated rat hepatocytes, isolated perfused rat liver and the rat in vivo. The anticipation of transport interactions at the hepatic clearance level should be based on data on the relative affinities of interacting substrates for the transport systems involved along with knowledge on the pharmacokinetics of these agents as well as the chosen dose regimen in the studied species. This review highlights the importance of multispecific tranporter systems such as OATP, accommodating a broad spectrum of organic compounds of various charge, implying potential transport interactions that can affect body distribution and organ clearance.

Animals↗
PubMed2004

The rat Ruby ( R) locus is Rab38: identical mutations in Fawn-hooded and Tester-Moriyama rats derived from an ancestral Long Evans rat sub-strain.

Hermansky-Pudlak syndrome (HPS) is a group of rare, recessive disorders in which oculocutaneous albinism, progressive pulmonary fibrosis, bleeding diathesis, and other abnormalities result from defective biogenesis of multiple cytoplasmic organelles. Seven different HPS genes are known in humans; in mouse, at least 16 loci are associated with HPS-like mutant phenotypes. In the rat, only two HPS models are known, Fawn-hooded (FH) and Tester Moriyama (TM), non-complementing strains in which HPS-like hypopigmentation and platelet storage pool deficiency result from a mutation of the Ruby (red eyed dilution; R) locus on Chromosome (Chr) 1. We have identified the R locus as the Rab38 gene, establishing that rat R is homologous to mouse chocolate ( cht). Further, we show that FH and TM rats have identical Rab38 Met1Ile mutations, occurring on an identical Chr 1 marker allele haplotype, indicating that these two strains derive from a common ancestor. This ancestor appears to have been a sub-strain of the outbred Long Evans (LE) strain, and several modern LE sub-strains carry the Rab38 Met1Ile R mutation on the same Chr 1 marker haplotype. These findings have significant implications for the many past and ongoing studies that involve the FH and LE-derivative rat strains. Hermansky-Pudlak syndrome (HPS; MIM 203300) is a group of autosomal recessive diseases in which oculocutaneous albinism (OCA), progressive and fatal pulmonary fibrosis, and bleeding diathesis due to platelet storage pool deficiency result from defects in the biogenesis of specific cytoplasmic organelles and granules: melanosomes, lysosomes, and platelet dense granules. In humans, seven different HPS genes are known. In the mouse, at least 16 loci associated with HPS-like mutant phenotypes are known, seven of which are homologous to the human HPS loci.

Animals↗
PubMed2003

Transthoracic echocardiography in rats. Evalution of commonly used indices of left ventricular dimensions, contractile performance, and hypertrophy in a genetic model of hypertrophic heart failure (SHHF-Mcc-facp-Rats) in comparison with Wistar rats during aging.

Two-weekly echocardiographic examinations were conducted in nine SHHF-Mc-fa(cp) rats in comparison with eight age-matched Wistar rats. In the SHHF-rats, characterized by progressive LV-dilation and decreasing contractile function between 77-87 weeks of age, left ventricular (LV) hypertrophy was most sensitively demonstrated by increased LV-mass-index (p < 0.001). LV-areas and area-ejection fraction (EF) (2D-images) discriminated more sensitively in the early stages than M-mode-derived diameters and fractional shortening (FS); midwall shortening was the most sensitive parameter of reduced systolic function. Post-mortem measurements showed an excellent correlation with calculated LV-mass (r = 0.91). Post-mortem LV-volumes correlated significantly with diastolic LV-diameters, LV-areas, and calculated LV-volumes (r = 0.56-0.59). Mean within-subject standard deviations in controls were 0.5-0.6 mm (LV-diameters), 3.1-4.6 mm(2) (LV-areas), approximately 10% of the mean for FS, area-EF and midwall shortening, and approximately 20% for wall thickness and LV-mass. The data might be used to choose the most sensitive parameters, and to estimate sample size for echocardiographic investigations in rats.

Aging↗
PubMed1997

Localization of rat CD1 transcripts and protein in rat tissues--an analysis of rat CD1 expression by in situ hybridization and immunohistochemistry.

CD1 molecules are cell surface glycoproteins non-covalently associated with beta2-microglobulin. Recently, functional features of the CD1 family such as a target ligand and an antigen-presenting structure for T cells have been reported. In the current study, tissue distribution of rat CD1 was analysed by in situ hybridization (ISH) in conjunction with immunohistochemistry to clarify the precise localization of both transcripts and proteins. CD1 transcripts were detected by ISH in a variety of organs: spleen, thymus, liver, lung, heart, kidney, small intestine and skin. In most organs, CD1 immunoreactivity paralleled the amount of CD1 mRNA expression and was localized in the same regions as its gene transcripts. However, there was a clear difference between the level of rat CD1 transcription and protein expression in the small intestine. CD1 mRNA was detected in the enterocytes of crypts of Lieberkuhn, but not in those of the intestinal villi, while immunoreactivity of CD1 protein was observed in the cells of the intestinal villi but not in those of crypts of Lieberkuhn. This suggests that CD1 gene transcription occurs in the enterocytes of intestinal crypts, and that as the cells of intestinal crypts migrate from the crypts to the intestinal villi, CD1 proteins are synthesized and accumulated in the intestinal villi. Such CD1 expression in the enterocytes appears to be consistent with migration-associated differentiation, and suggests that rat CD1 may take part in mucosal immunity as a first line of defence. In addition, clear cell membrane CD1 immunoreactivity on lymphoid cells raises the possibility that intercellular interaction via rat CD1 and T cell receptors may be involved in both lymphoid cell differentiation and immunoregulation.

Animals↗
PubMed1982

The antiandrogenic effects of delta 1-testolactone (Teslac) in vivo in rats and in vitro in human cultured fibroblasts, rat mammary carcinoma cells, and rat prostate cytosol.

The antiandrogenic properties of delta 1-testolactone (17 alpha-oxa-D-homo-1,4-androstane-3,17-dione; Teslac) were investigated in vivo and in vitro. Teslac (75 mg/day for 7 days) inhibited the rise in ventral prostate weight induced by testosterone (T) (P less than 0.001), dihydrotestosterone (DHT) (P less than 0.05), and a combination of T plus 17 beta-estradiol (E2) (P less than 0.01) in immature castrate rats. Similar effects were seen on the seminal vesicles after T and T plus E2 (P less than 0.001). Teslac also decreased prostate and seminal vesicle weights in intact immature rats. The effects of Teslac were dose and time dependent. Teslac did not change the concentration of serum T or DHT. However, Teslac inhibited DHT binding to the androgen receptor (Ki = 2.5 +/- 0.8 X 10(-7) M) in cytosol of the rat prostate. Teslac also inhibited DHT binding to the androgen receptor in cultured human prepuce fibroblasts and cultured rat mammary tumor cells (Ki = 1.9 +/- 0.3 X 10(-5) M). The results indicate that Teslac, in addition to its antiaromatase activity, is an antiandrogen by virtue of its interaction with the androgen receptor.

Androgen Antagonists↗
PubMed1992

Localization of bFGF mRNA in cyclic rat ovary, diethylstilbesterol primed rat ovary, and cultured rat granulosa cells.

Evidence from in vitro studies strongly implicates basic fibroblast growth factor (bFGF) as a local regulator of ovarian function. However, the in vivo function of this growth factor in the ovary is uncertain. The objective of this study has thus been to investigate the biological role of bFGF in the rat ovary by monitoring bFGF gene expression using in situ hybridization in 3 systems; (1) the naturally cycling ovary, (2) ovaries of immature rats treated with diethylstilbesterol (DES), and (3) primary rat granulosa cell cultures. The rat estrus cycle can be divided into 4 stages as determined by vaginal cytology; diestrus, proestrus, estrus and metestrus. bFGF mRNA transcripts were localized to granulosa and theca cells of developing follicles during proestrus and estrus and in the corpus luteum following ovulation during metestrus. The estrogen analogue DES induced extensive in vivo folliculogenesis and high levels of bFGF mRNA in both granulosa and theca cells when compared to controls. Detectable levels of bFGF mRNA were also observed in primary granulosa cell cultures grown to high density. Employment of this in situ hybridization procedure has enabled the in vivo cellular sources of bFGF mRNA to be identified and the time course of expression during the estrus cycle to be monitored. The biological significance of this expression and the interplay between bFGF, extra- and intra-ovarian modulators are discussed.

Animals↗
PubMed1986

Leucocyte surface antigens in metrial gland tissue of ovariectomized pregnant rats, deciduomata-bearing rats and in uterine tissue of non-pregnant rats.

The effects of withdrawal of ovarian hormones and absence of paternal antigens on numbers and distribution of cells expressing Ia, Thy 1.1 or leucocyte-common (LC) antigens in the rat metrial gland have been assessed. The distribution of these markers in non-pregnant uterus at various stages of the oestrous cycle has also been investigated. In primigravid rats at Day 15 of gestation, following ovariectomy on Day 12, marker distribution was not different from that in uninterrupted pregnancy. However, there was a significant increase in the percentage of cells expressing LC antigen, which was not accompanied by an increase in the percentage of the glycoprotein-containing, LC antigen-positive granulated metrial gland (GMG) cells. It was suggested that the accumulation of LC antigen-positive, non-GMG cells might represent the precursors of GMG cells. In deciduomata-bearing rats, there was a significantly lower percentage of LC antigen-bearing cells at Day 13 of pseudopregnancy than in pregnant rats at Day 13, but no difference in the percentages of GMG cells was noted. Cells expressing Ia, LC or Thy 1.1 antigens were detected in the endometrial stroma, surrounding endometrial glands and the luminal epithelium of the non-pregnant uterus.

Animals↗
PubMed1997

Long-term blockade of the angiotensin II receptor in renin transgenic rats, salt-loaded Dahl rats, and stroke-prone spontaneously hypertensive rats.

These studies were designed to investigate the protective effects of the new angiotensin II receptors antagonist BAY 10-6734 (6-n-butyl-4-methoxycarbonyl-2-oxo-1[(2'-(1H-tetrazol-5-yl) -3-fluorobiphenyl-4-yl)methyl] 1,2-dihydropyridine, CAS 156001-18-2) on haemodynamic, hormonal, renal, and structural parameters in renin transgenic rats (TGR(mRen2)27), salt-loaded Dahl S and R rats, and salt-loaded stroke-prone spontaneously hypertensive rats (SHR-SP) in long-term trials. Study 1: In SHR-SP the development of blood pressure, cardiac hypertrophy, and the deleterious effects of salt loading on kidney structure and kidney function was prevented by BAY 10-6734. Study 2: In salt-loaded Dahl S rats with a suppressed plasma renin activity treatment with BAY 10-6734 did not delay the increase in blood pressure but prevented cardiac hypertrophy and the increase in plasma ANP (Atrial natriuretic peptide). Study 3: TGR develop malignant hypertension associated with cardiac hypertrophy, elevated left-ventricular end-diastolic pressure and increased plasma ANP. After 6 weeks of treatment with BAY 10-6734 (30 mg/kg p.o. bid) cardiac pump function was improved and cardiac hypertrophy was reversed in this angiotension dependent form of hypertension. The beneficial effects of BAY 10-6734 in these different animal hypertension models are also emphasized by a reduction in mortality.

Aldosterone↗
PubMed1997

Antitumor activity of carcinoma-reactive BR96-doxorubicin conjugate against human carcinomas in athymic mice and rats and syngeneic rat carcinomas in immunocompetent rats.

The internalizing monoclonal antibody BR96 was conjugated to the anticancer drug doxorubicin (DOX) using an acid-labile hydrazone bond to DOX and a thioether bond to the monoclonal antibody. The resulting conjugate, termed BR96-DOX, binds to a tumor-associated Lewis(y) antigen that is abundantly expressed on the surface of human carcinoma cells. BR96-DOX binds to RCA, a human colon carcinoma cell line, and BN7005, a transplantable colon carcinoma induced in a Brown Norway (BN) rat by 1,2-dimethyl-hydrazine. BR96-DOX produces cures of established s.c. RCA human colon carcinomas in athymic mice and rats. BR96-DOX also cured both s.c. and intrahepatic BN7005 tumors in immunocompetent BN rats. Unconjugated DOX, given at its maximum tolerated dose, and matching doses of nonbinding IgG-DOX conjugate were not active against RCA or BN7005 carcinomas. An anticonjugate antibody response was produced in BN rats treated with BR96-DOX. However, this could be largely prevented by administering the immunosuppressive drug deoxyspergualin. These results confirm the concept of antibody-directed therapy in models in which the targeted antigen is expressed both in normal tissues and tumors. The findings in BN7005 further demonstrate efficacy of BR96-DOX therapy in a model in which the tumor is syngeneic and the host is immunocompetent.

Adenocarcinoma↗
PubMed1980

Phenolic ring deiodination in cultured rat hepatoma cells, and subcellular localization of deiodinases in cultured rat hepatoma, monkey hepatocarcinoma cells and normal rat liver homogenates.

The cultured rat hepatoma cell (R117--21B) homogenates metabolized 3,[3',5'-125I]triiodothyronine by phenolic ring deiodination and produced radioactive iodide and 3,3'-diiodothyronine. Thyroxine (T4) was converted to 3,3',5-triiodothyronine (T3). The production of 125I- represented the deiodination was observed to be pH 6.0--7.0. This enzyme reaction was accelerated by dithiothreitoil. Propylthiouracil strongly inhibited the phenolic ring deiodination at 0.1 mM, whereas an effect of 20 mM methylmercaptoimidazol on the deiodination was very weak or absent. Excess unlabeled iodothyronines (T4, T3 and 3,5-diiodo-L-thyronine) inhibited the phenolic ring deiodination of labeled 3,3',5'-triiodothyronine, although their inhibitory effect was slightly different. Triiodothyroacetic acid was a better inhibitor than T3. Diiodotyrosine did not affect phenolic ring deiodination in cultured rat hepatoma cell homogenates. Phenolic and nonphenolic ring deiodinase activities of cultured monkey hepatocarcinoma cell and rat liver homogenates were also studied by the use of 3,[3',5'-125I]triiodothyronine and [3,5-125I]thyroxine, respectively. Both deiodinase activities were observed in particulate fractions (mitochondrial and microsomal) of cultured cell and rat liver homogenates.

Animals↗
PubMed1975

Concanavalin A receptors on normal rat liver cells, on rat liver cells in vivo transformed by diethylnitrosamine and on Zajdela ascites hepatoma cells of the rat: morphokinetic analysis of cell surface dynamics.

Comparative electron microscopic investigations were performed in living cultures of normal rat liver cells, of rat liver cells in vivo transformed by diethylnitrosamine and on Zajdela ascites hepatoma cells of the rat concerning the mobility of the Concanavalin A cell surface receptors. The cells were incubated in Concanavalin A and peroxidase and subsequently washed. They were then reincubated for various periods at +37 degrees C in PBS prior to fixation. In the case of the Zajdela ascites hepatoma cells the cells were reincubated after Concanavalin A incubation followed by fixation and peroxidase incubation. The cytochemical procedure allowed us to show differences in the mobility of Concanavalin A surface receptors between normal and transformed rat liver cells. The cell surface label disappeared completely within 15 min of reincubation in the transformed cells, whereas in normal cells the same degree of loss in surface label was visible after 120 min reincubation. In both cases an internalization of labelled plasma membrane areas occurred. After complete disappearance of cell surface label in diethylnitrosamine transformed cells a complete relabelling of the cell surface occurred after 60 min reincubation caused by an exocytosis.

Animals↗
PubMed1968

The metabolism of glucose in diaphragm muscle from normal rats, from streptozotocin-treated diabetic rats and from rats treated with anti-insulin serum.

1. The metabolism of [U-(14)C]glucose by the isolated diaphragm muscle of normal rats, rats rendered diabetic with streptozotocin and rats with transitory insulin deficiency after an injection of anti-insulin serum was studied. 2. The incorporation of [(14)C]glucose into glycogen and oligosaccharides was significantly decreased in the diabetic diaphragm muscle and in the muscle from rats treated with anti-insulin serum. 3. Neither diabetes nor transitory insulin deficiency influenced the oxidation of glucose, or the formation of lactate and hexose phosphate esters from glucose. 4. Insulin fully restored the incorporation of glucose into glycogen and maltotetraose in the diabetic muscle, but the incorporation into oligosaccharides, although increased in the presence of insulin, was significantly lower than the values obtained with normal diaphragm in the presence of insulin.

Animals↗