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Biomedical subjects

D B Martin

Publications and source records attributed to D B Martin.

At least 37 records · Page 2Linked to original sources
PubMed1981

Enhancement of ketosis by 16,16 dimethylprostaglandin E2 during the genesis of diabetic ketoacidosis in rats.

We examined the effects of 16,16 dimethylprostaglandin E2 (DMPGE2) on the development of diabetic ketoacidosis (DKA) in rats. Animals received DMPGE2, 200 or 300 microgram/kg body weight subcutaneously in 0.5 ml saline, or the saline carrier alone at 0, 12, 24 and 36 hours after administration of streptozotocin. At 40 hours, blood was obtained for measurement of plasma free fatty acids (FFAs) and ketone bodies. DMPGE2 produced a dose-related decrease in plasma FFA levels at 40 hours. FFA levels were 2.76 +/- 0.39 meg/L (mean +/- SEM) with saline, 1.72 +/- 0.22 meg/L with 200 microgram/kg DMPGE2 (p less than 0.05 vs saline) and 1.19 +/- 0.17 meg/L with 300 microgram/kg DMPGE2 (p less than 0.025 vs saline) consistent with the previously demonstrated antilipolytic effect of DMPGE2 in vivo and in vitro. Despite suppression of lipolysis, DMPGE2 enhanced the development of ketosis during the genesis of DKA. The beta-hydroxybutyrate level was 5.89 +/- 0.06 mM with saline, 8.15 +/- 1.02 mM with 200 microgram/kg DMPGE2 and 11.17 +/- 0.60 mM with 300 microgram/kg DMPGE2 (p less than 0.001 vs saline). This study demonstrates that this analog of prostaglandin E2 promotes the development of ketosis during the genesis of DKA despite decreased substrate availability. This may be due to enhancement of hepatic ketogenesis, impairment of ketone disposal, or both.

Animals↗
PubMed1980

Subarachnoid hemorrhage--the initial manifestation of bacterial endocarditis. Report of a case with negative arteriography and computed tomography.

The case of a patient who suffered a nontraumatic subarachnoid hemorrhage (SAH) associated with normal angiography is reported. Three weeks later he developed an embolic stroke secondary to a nonhemolytic Staphylococcus epidermidis endocarditis of the mitral valve; thus, the SAH was the initial manifestation of bacterial endocarditis. Bacterial endocarditis should be considered a possible cause of SAH, especially in the 7% of patients with angiographically negative SAH.

Adult↗
PubMed1980

The detection of islet-cell antibodies by immunofluorescence in Bouin's-fixed, paraffin-embedded human pancreas.

Pancreatic islet-cell antibodies have been demonstrated in the sera of insulin-dependent diabetic patients, with or without polyendocrine disease, by immunofluorescent microscopy in which cryostat sections of fresh-frozen human pancreas were used as the substrate. In the present study we used sections of Bouin's-fixed, paraffin-embedded, trypsin-treated human pancreas as the islet-cell substrate and compared the results to those obtained with cryostat sections. Twenty-four sera from insulin-dependent diabetic patients, one serum from a non-insulin dependent diabetic patient and five sera from normal individuals were tested. With serum samples containing islet- cell antibodies, Bouin's-fixed, paraffin-embedded tissue produced a more intense fluorescence, was easier to use and was more sensitive than the conventional cryostat method.

Acetates↗
PubMed1979

Atypical measles in adolescents and young adults.

Seven patients, aged 12 to 19 years, had atypical measles. Prodromal symptoms of fever, malaise, myalgia, headache, nausea, and vomiting were commonly followed by coryza, sore throat, conjunctivitis, photophobia, nonproductive cough, and pleuritic pain. The characteristic rash was erythematous, maculopapular, and progressed frequently to vesicular, petechial, or purpuric lesions. It initially involved palms and soles with subsequent spread to proximal extremities and the trunk, sparing the face. Six of six chest roentgenograms showed infiltrates. Findings not previously described in atypical measles included liver enzyme elevations, thrombocytopenia, disseminated intravascular coagulation, possible transmission among three siblings, and suspected cardiac involvement. Measles complement fixation titers compatible with recent infection were seen in all patients. All patients had previously received killed measles vaccine. A substantial number of persons who are older adolescents or young adults may be at risk of developing atypical measles.

Adolescent↗
PubMed1976

Identification and subcellular distribution of adipocyte peptides and phosphopeptides.

Subcellular fractions of high purity (including plasma membrane, endoplasmic reticulum, mitochondria, nuclei, and cytoplasm) were prepared from isolated adipocytes, and the peptide components were examined by detergent gel electrophoresis. Each fraction except the endoplasmic reticulum exhibited a unique and reproducible complement of major peptides. Although the endoplasmic reticulum was distinctive in its enzymic markers, its peptide components showed striking homologies with certain species in the plasma membrane and cytoplasm. The two major adipocyte glycopeptides appear to be contained in the plasma membrane, inasmuch as they followed the distribution of 5'-nucleotidase. Incubation of adipocytes with extracellular 32Pi led to a uniform rate of incorporation of 32P into cellular peptides, with steady-state incorporation reached by 2 hours. Plasma membrane, mitochondria, nuclei, and cytoplasm all contained a distinctive complement of from two to five major phosphopeptides of different molecular weights. The majority of endoplasmic reticulum phosphopeptides exhibited molecular weights closely similar to those of certain species in the plasma membrane and cytoplasm. The phosphopeptides of the plasma membrane exhibited the highest absolute 32P incorporation of all phosphopeptides, next was the single major mitochondiral phosphopeptide. All fractions except the mitochondria contained, in addition to the few major phosphopeptides, numerous minor 32P-labeled phosphopeptides.

Adipose Tissue↗
PubMed1976

Effects of epinephrine and insulin on phosphopeptide metabolism in adipocytes.

Isolated adipocytes, incubated in the presence of extracellular 32Pi to steady state 32P incorporation into cellular phosphopeptides, were exposed to hormones for 5 min. Epinephrine (10(-6) M) stimulated 32P incorporation into at least 12 major phosphopeptides, distributed in the cytoplasm, endoplasmic reticulum, and plasma membrane. Quantitatively pre-eminent among these were peptides of molecular weight 123,000 and 69,000, each located both in the cytoplasm and endoplasmic reticulum. The effect of epinephrine (10(-7) M) on 32P incorporation into these two peptides was augmented by theophylline (10(-3) M) in a synergistic fashion. Norepinephrine, dibutyryl N6,O2'-dibutyryl adenosine 3':5'-monophosphate, adrenocorticotropic hormone (ACTH) (synthetic 1 to 24 fragment), and glucagon mimicked the effect of epinephrine. Insulin modified adipocyte peptide phosphorylation in two ways. When present as the sole hormone, insulin (100 microunits/ml) consistently and selectively stimulated the 32P incorporation into a peptide of molecular weight 123,000 (endoplasmic reticulum, cytoplasm) without significant alteration in the 32P content of any other major peptide. A second effect of insulin was evident when epinephrine (10(-6) M) was present simultaneously. Insulin significantly inhibited the epinephrine-stimulated phosphorylation of the molecular weight 69,000 (endoplasmic reticulum, cytoplasm) and 26,000 (plasma membrane) peptides. Nevertheless, persistence of insulin-stimulated phosphorylation of the 123,000 peptide in the presence of epinephrine was shown by a 32P content of this peptide that was greater in the presence of both hormones than with either individually. These findings indicate that in intact adipocytes: (a) epinephrine acutely alters the phosphorylation of a large number of adipocyte peptides, partly at least, via activation of adenosine 3':5'-monophosphate (cyclic AMP)-dependent protein kinase; (b) insulin opposes several epinephrine-stimulated phosphorylations in a manner consitent with its ability to lower epinephrine-stimulated intracellular cyclic AMP accumulation in adipocytes; and (c) insulin, in addition, exerts a unique stimulatory effect on adipocyte peptide phosphorylation that is independent of its effects on cyclic AMP metabolism and may be medicated by the generation of an as yet undefined intracellular "messenger" unique to insulin.

Adipose Tissue↗
PubMed1976

Glucagon secretion from the perfused pancreas of streptozotocin-treated rats.

One hour following intravenous streptozotocin, rat pancreases were perfused in situ, and , in contrast to saline-injected controls a marked decrease of insulin secretion was observed. In these streptozotocin-treated animals, baseline glucagon secretion was enhanced when the perfusate glucose concentration was either 80 mg./100 ml. or 300 mg./100 ml. In addition there was hypersecretion of glucagon in response to arginine. Exogenous insulin (20,000 muU./ml.) could suppress glucagon secretion when endogenous secretion was plentiful. Baseline and arginine-stimulated glucagon secretion of the streptozotocin treated animals was not suppressed by large amounts of glucose and insulin to the degree seen in control animals. The glucagon rise in response to an abrupt fall of glucose from 80 mg./100 ml. to 25 mg./100 ml. was not significantly higher in the control group than in the streptozotocin group. The results seen with epinephrine were in sharp contrast to those found with arginine. Epinephrine-stimulated glucagon secretion was not enhanced in the streptozotocin group. In addition, epinephrine-induced secretion could be suppressed by exogenous insulin in both the control and streptozotocin groups. The differences may be secondary to differences of endogenous insulin secretion. The present results are compatible with the hypothesis that local insulin secretion can exert a significant suppressive effect upon the alpha cell and that the inhibition of glucagon secretion by glucose is partially mediated by this mechanism. Furthermore, anomalous local insulin secretion may contribute to the abnormal glucagon secretion of diabetes mellitus.

Animals↗
PubMed1975

Nucleotide and nucleoside stimulation of glucagon secretion.

The effects of various nucleosides and nucleotides upon glucagon secretion from the isolated perfused rat pancreas were studied. Increasing glucagon secretion was found with increasing concentrations of exogenous cyclic AMP (2 X 10(-4) M, 2 X 10(-3) M and 1 X 10(-2) M). Stimulation of alpha cell secretion was also found with 2 X 10(-3) M 2'AMP, 3'AMP, 5'AMP, ADP, Adenosine, NADP, and NADPH. One X 10(-3) M cyclic GMP elicited significant glucagon secretion. The pattern of glucagon release was similar in all cases with peak secretion occurring during the 30- to 90-s time period following initiation of the stimulus. No significant increase of glucagon secretion was found in response to ATP, guanosine, 2'GMP, 3'GMP, 5'GMP, GTP, xanthosine, inosine, adenine, xanthine, thymidine, cytidine, ribose, nicotinamide, and uric acid. On the basis of the above results, the structural requirement for stimulation of glucagon secretion appears to be adenine linked to ribose, with phosphate groups being unnecessary. The conclusion of this study is that a new class of compounds capable of stimulating glucagon secretion has been identified, and important questions are thus raised about the mechanism of the action of exogenous cyclic AMP.

Animals↗
PubMed1975

High molecular weight glucagon-like immunoreactivity in plasma.

An "interference factor" has been shown to be present in human plasma, which can cause artifactual elevation of pancreatic glucagon values as conventionally determined by radioimmunoassay using antiserum 30K. A method of correcting for this problem was developed and used to measure glucagon levels in 60 diabetic and 30 nondiabetic subjects. No significant difference was found between the two groups. Twelve percent of the diabetic subjects had evidence of glucagon binding in their plasma which prevented valid measurement of their glucagon levels. Characterization of the "interference factor" was undertaken with G-200 sephadex column chromatography. Large amounts of glucagon-like immunoreactivity were found in fractions indicating an approximate molecular weight of 160,000. It was demonstrated that this "factor" was not an artifact of charcoal treatment of plasma. The original source of this material is unknown.

Blood Proteins↗
PubMed1974

Glucagon secretion from the perfused rat pancreas. Studies with glucose and catecholamines.

The isolated in situ perfused rat pancreas was used to study glucose and catecholamine control of glucagon secretion, and to investigate the possible role of endogenous cyclic AMP as a mediator of this secretory process. When perfusate glucose was acutely dropped from 100 to 25 mg/100 ml, glucagon was released in a biphasic pattern with an early spike and a later plateau-like response. 300 mg/100 ml glucose suppressed glucagon secretion to near the detection limit of the radioimmunoassay (15 pg/ml). When perfusate glucose was dropped from 300 to 25 mg/100 ml, a delayed, relatively small peak occurred suggesting persisting alpha cell suppression by prior high glucose exposure. 2-Deoxy d-glucose stimulated glucagon secretion and inhibited insulin secretion. Glucagon was secreted in a biphasic pattern in response to both 2.7 x 10(-7) M epinephrine and norepinephrine. The glucagon response to epinephrine was markedly suppressed by glucose at 300 mg/100 ml, and the biphasic response pattern was obliterated. Glucose evoked a two-phase insulin secretory pattern, and the second phase was markedly and rapidly inhibited by epinephrine. Pancreases were perfused with glucose at 300 mg/100 ml which was then lowered to 80 mg/100 ml. 5 min later, epinephrine was infused and definite blunting of the first-phase spike occurred. 10 mM theophylline produced modest rapid uniphasic stimulation of glucagon release, and, in addition, caused enhancement of epinephrine-stimulated glucagon release. An inhibitory influence upon epinephrine-stimulated glucagon was observed as well. Insulin secretion was stimulated by 10 mM theophylline, and this stimulation was inhibited by epinephrine.

Animals↗