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Biomedical subjects

K M Shakir

Publications and source records attributed to K M Shakir.

At least 55 records · Page 3Linked to original sources
PubMed1982

Inhibition of phospholipase A2 activity by Fluosol, an artificial blood substitute.

This paper describes the effect of Fluosol on phospholipase A2 activity both in vitro and in vivo. This compound inhibited both postheparin plasma and hepatic phospholipase A2 activities. Furthermore, in Fluosol transfused rats the postheparin plasma phospholipase A2 activity was 41% below that observed in control animals. The inhibition of phospholipase A2 activity was due to the micellar forms of pluoronic, F-68, a detergent present in Fluosol. It is postulated that the inhibition of phospholipase A2 activity by Fluosol might interfere with the release of arachidonic acid, a substrate used in biosynthesis of prostaglandins.

Animals↗
PubMed1982

Intestinal phospholipase A and triglyceride lipase: localization and effect of fasting.

We investigated the distribution of phospholipase A and triglyceride lipase in the rat small intestine and the effects of heparin and hormones on enzyme release. Phospholipase A activity was 10 times higher in the ileum than in the jejunum; triglyceride lipase activity was threefold higher in the jejunum than in the ileum. Activities of both enzymes were much greater in villus than in crypt cells. The specific activity of phospholipase A was highest in microsomes and least in cytosol. The crude nuclei and brush-border fraction contained 40.5% of total phospholipase A activity; mitochondria contained 33.8%; and microsomes, 17.4%. Phospholipase A activity increased significantly in the distal intestinal mucosa in fasted rats compared with controls. Heparin did not increase the release of phospholipase A by isolated intestinal cells or perfused intestinal vasculature. Thus, the small intestine probably does not contribute significantly to the phospholipase A activity of postheparin plasma. Hormones and cAMP, which inhibit the secretion of phospholipase A and triglyceride lipase from isolated hepatocytes, had no effect on the release of either enzyme from intestinal cells.

Alkaline Phosphatase↗
PubMed1978

Release of phospholipase A and triglyceride lipase from rat liver.

A new, rapid, and sensitive assay for phospholipase A, utilizing commercially available [14C]phosphatidylethanolamine with 14C label in both palmitic acid moieties, was used to study phospholipase A release from perfused liver, hepatocytes, and intestinal cells from rats. Heparin triggered a prompt release of phospholipase A from perfused liver. Phospholipase A and triglyceride lipase were released from hepatocytes at a linear rate for 1 h and 30 min, respectively. Heparin (20 u/ml) doubled the release of phospholipase A and triglyceride lipase from hepatocytes. Colchicine (0.1 mM), but not puromycin (0.2 mM), inhibited basal and heparin-stimulated phospholipase A release by 40%. Since the amount of phospholipase A and triglyceride lipase released into the medium greatly exceeded intracellular activities, it is possible that secretion is coupled with intracellular conversion from inactive to active forms of the enzymes. Dibutyryl cyclic AMP (1 mM) inhibited phospholipase A (48%) and triglyceride lipase (82%) release from hepatocytes. Epinephrine, dexamethasone, and clofibrate inhibited release of triglyceride lipase but not phospholipase A. Phospholipase A activity of intestinal cells was greater than in hepatocytes, but neither heparin nor dibutyryl cyclic AMP affected phospholipase A release from intestinal cells. These results suggest that the liver is a major source of phospholipase A of postheparin plasma. The fact that dibutyryl cyclic AMP affects the release of these enzymes suggests an additional mechanism for hormonal regulation of lipid and lipoprotein metabolism.

Animals↗
PubMed1978

Association of diamine oxidase and ornithine decarboxylase with maturing cells in rapidly proliferating epithelium.

Diamine oxidase and ornithine decarboxylase activities are shown to have a parallel distribution across rat small intestine mucosa; levels of both enzyme activities are sharply higher in mature cells in the villus tip region than in proliferating cells in the crypt areas. Histidine decarboxylase levels were not measurable in the same cell preparations and aromatic-L-amino-acid decarboxylase activity was distributed in an opposite pattern to diamine oxidase and ornithine decarboxylase. The results suggest that intestinal diamine oxidase could be involved with polyamine metabolism. The new findings for ornithine decarboxylase suggest an in vivo role for polyamines in non-proliferative cells; rat small intestinal mucosa may be an excellent model for investigating the function of polyamines in regenerating cells.

Amine Oxidase (Copper-Containing)↗
PubMed1978

Lipid synthesis in isolated intestinal cells.

Since the small intestine contributes significantly to serum cholesterol and very low density lipoprotein levels, acute regulation of lipid synthesis was investigated in isolated rat intestinal cells incubated in Krebs-Ringer bicarbonate buffer with 5 mM glucose and [14c]acetate or 3H2O. Incorporation of [14c]acetate into cellular lipids was 6- to 8-fold greater in crypt than in villus cells. In both cell types the distribution of 14C among the various lipid classes was as follows: 52.5% in triglycerides, diglycerides, and monoglycerides; 22.3% in cholesterol; 8.3% in cholesteryl esters; 1.9% in fatty acids; and 15.0% in phospholidpids. In contrast, the medium lipids contained significantly higher amounts of tri-, di- and monoglycerides (61.1%) and lower amounts of cholesteryl esters (2.3%) and phospholipids (11.9%). After saponification, 2/3 of the recovered 3H2O was in fatty acids and 1/3 in cholesterol. Ethanol (10 mM) tripled 3H2O incorporation into cellular lipids but had no effect on [14c]acetate incorporation. Epinephrine and norepinephrine (10 micron), glucagon (10 micron), dibutyryl cyclic AMP (1MM), dexamethasone (1 mM and 1 micron), and cholera toxin (1 microgram/ml) did not affect [14c]acetate incorporation. We concluded that ehtanol stimulates intestinal lipid synthesis; however, in sharp contrast to their inhibition of lipid synthesis in hepatocytes and adipocytes, catecholamines, glucagon, and dibutyryl cyclic AMP do not inhibit lipid synthesis in intestinal cells.

Acetates↗
PubMed1976

Hyperlipoproteinemia: diagnosis and management.

The hyperlipidemias are fairly common and require proper understanding. They may cause major complications, they may present as secondary manifestations of a number of common diseases, and, finally, a diagnosis of primary hyperlipidemia has significant implications for the patient's family.

Adolescent↗
PubMed1975

Effect of thyroid hormone on metabolic adaptation to fasting.

The acute effect of triiodothyronine (T3) on mobilization of fat and protein energy stores has been measured in five fasting, normal men. Fasting subjects were chosen for this study to amplify catabolic effects occurring during brief thyroid hormone treatment. Subjects were fasted for 72 hr on two occasions with admintration of T3, 150 mug every 12 hr, for 72 hr before and during the second fast. Plasma beta hydroxybutyrate, acetoacetate, and free fatty acid levels as well as ketone, creatine, and urea excretion were measured during control and T3 fasts. T3 enhances catabolism of protein stores as indicated by the doubling of urea excretion during the T3 fasts. Likewise, creatine excretion is increased six to ninefold during the T3 fasts. Catabolism of fat stores is enhanced during the T3 fasts as shown by increased plasma free fatty acid and ketone levels, and increased ketone excretion. Brief T3 treatment for 3 days augments the expected protein and fat catabolism of starvation without causing subjective changes of hyperthyroidism. Much of the catabolic expression of hyperthyroidism may simply reflect inadequate caloric intake to fuel energy requiring processes stimulated by thyroid hormone such as cell membrane sodium pumping and protein synthesis.

Adult↗
PubMedDate not supplied

Monensin inhibition of corticotropin releasing factor mediated ACTH release.

Monensin is a sodium selective carboxylic ionophore that has been helpful in studying the intracellular mechanisms of protein secretion by its ability to inhibit transport of secretory proteins, particularly through the Golgi apparatus, and by its capacity to block intracellular posttranslational processing events. We studied in rat anterior pituitary cell culture the effects of monensin on: CRF stimulated ACTH release; presynthesized (stored) ACTH release; and on forskolin- (activator of adenylate cyclase) and KCl- (a membrane depolarizer which does not stimulate ACTH synthesis) induced ACTH release. Monensin inhibited CRF stimulated ACTH release in a dose-dependent fashion. The ED50 was 2.7 x 10(-8) M and maximal inhibition was 52% at 1.5 x 10(-7) M. Inhibition at 40 minutes of CRF incubation was similar to the percent inhibition noted at 1 hr 40 min and 2 hr 40 min. Monensin (1.5 x 10(-6) M) decreased the amount of ACTH release from cells incubated with cycloheximide plus CRF by 32% (p less than 0.01). Monensin individually inhibited forskolin (2 x 10(-6) M) and dibutyryl cyclic AMP (3 x 10(-3) M) mediated ACTH release in a dose-dependent fashion. The inhibition of forskolin and dibutyryl cyclic AMP mediated ACTH release by 1.5 x 10(-6) M monensin was 48% and 46% respectively. Monensin (1.5 x 10(-6) M) also reduced KCl (50 mM) stimulated ACTH release by 48%. This study demonstrates that monensin inhibits CRF mediated ACTH release.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Impotence as a presenting symptom of presumed prolactinoma in a patient with diabetes mellitus.

Impotence in diabetic men is usually considered to be due to neuropathic factors or vascular insufficiency. However, factors unrelated to diabetes may occasionally produce sexual dysfunction in these patients. Recently, a diabetic patient presented to our clinic with the complaint of impotence. In this patient, macroprolactinemia was discovered. With appropriate therapy, the sexual dysfunction improved and this case is reported here.

Diabetes Mellitus, Type 1↗
PubMedDate not supplied

Postsplenectomy sepsis caused by group B streptococcus (S. agalactiae) in an adult patient with diabetes mellitus.

Overwhelming postsplenectomy infection (OPSI) due to group B streptococcus developed in an insulin-dependent diabetic patient. The illness began with nonspecific symptoms, followed rapidly by hypotension and disseminated intravascular coagulation. The early institution of appropriate antibiotics, fluid replacement and pressor agents resulted in a favorable clinical outcome. The association of group B streptococcal infection and diabetes mellitus is discussed. The defects in normal host defenses associated with asplenic state and diabetes mellitus are further emphasized. This is the first case report linking the association of OPSI, diabetes mellitus and group B streptococcal septicemia.

Adult↗
PubMedDate not supplied

Exacerbation of warfarin-induced anticoagulation by hyperthyroidism.

OBJECTIVE: To alert clinicians to the potential interaction between warfarin and hyperthyroidism. METHODS: We present two case reports and compare findings with those in a control population of patients with hyperthyroidism who were not receiving anticoagulant therapy. RESULTS: In two patients, severe coagulopathy was precipitated by the interaction of warfarin and increased thyroid hormone levels. In both cases, the patients also demonstrated resistance to vitamin K therapy, which persisted for several days. We also studied five control patients with hyperthyroidism who were not taking anticoagulant drugs; no effect of thyroid hormone on the plasma levels of vitamin K-dependent clotting factors was noted. One of our patients with hyperthyroidism who was taking warfarin had levels of warfarin in the serum that were 5 times the therapeutic range; this finding suggests that the protein binding or absorption of warfarin may be altered in such patients. CONCLUSION: Multiple factors may contribute to the enhanced effect of warfarin seen in patients with hyperthyroidism, including altered metabolism of vitamin K-dependent clotting factors, altered metabolism of warfarin, or decreased protein binding of the drug. Patients with hyperthyroidism should be given lower doses of warfarin to avoid severe coagulopathy.

Journal Article↗
PubMedDate not supplied

Ward's triangle bone mineral density determined by dual-energy x-ray absorptiometry is a sensitive indicator of osteoporosis.

OBJECTIVE: To assess the clinical utility of bone mineral density (BMD) of Ward's triangle by dual-energy absorptiometry (DEXA) as an indicator of osteoporosis in comparison with quantitative computed tomography (QCT) of the lumbar spine and DEXA of the lumbar spine and hip sites (trochanter and femoral neck). METHODS: We conducted a retrospective study of all patients (28 men and 17 women) with decreased BMD by QCT (T-score less than -1.0) who had DEXA BMD performed at the lumbar spine and hip between October 1993 and January 1995 in our Endocrine Clinic. RESULTS: Osteoporosis based on the World Health Organization criteria (T-score less than -2.5) was defined by QCT lumbar spine BMD in 78% of the study subjects and by DEXA of Ward's triangle in 53%, of the femoral neck in 22%, of the trochanter in 7%, and of the lumbar spine in 2%. In the men, the only DEXA BMD measurement that was sensitive for detecting osteoporosis was Ward's triangle. Of the 24 men with osteoporosis by QCT BMD, 14 were defined as having osteoporosis by DEXA exclusively at Ward's triangle. The DEXA lumbar spine BMD measurement was actually above the mean for young normal control subjects in 8 of the 24 men with osteoporosis by QCT BMD. In the 11 women with osteoporosis by QCT BMD, the DEXA BMD at Ward's triangle and the femoral neck were equally sensitive in detecting osteoporosis, whereas the DEXA lumbar spine and trochanter BMD measurements were insensitive. CONCLUSION: DEXA BMD of Ward's triangle is a sensitive indicator of osteoporosis, particularly in men, and should be used to identify patients at increased risk for osteoporosis-related fractures.

Journal Article↗
PubMedDate not supplied

Effect of alendronate treatment on bone mineral density in male patients with osteoporosis.

OBJECTIVE: To assess the efficacy of alendronate therapy on bone mineral density (BMD) at the lumbar spine and hip in men with osteoporosis. METHODS: Medical records of male patients with osteoporosis, who had undergone follow-up in the Endocrinology Clinic at the National Naval Medical Center, were reviewed, and nine patients treated with alendronate for at least 1 year were identified. Patients were excluded from analysis if they had evidence of osteomalacia or if baseline and follow-up BMD results on the same dual-energy x-ray absorptiometry (DEXA) densitometer, at least 10 months apart, were not available. DEXA BMD results at the lumbar spine and hip, before and after at least 10 months of alendronate treatment, were analyzed for significant differences. Patients were also receiving calcium supplementation (1,000 to 1,500 mg/day), and all but one patient received vitamin D (400 to 800 U/day). RESULTS: Lumbar spine BMD increased by 6.4 +/- 1.8% per year with alendronate treatment (P = 0.008). A mean absolute gain of 0.052 +/- 0.010 g/cm 2 (P = 0.005) in lumbar spine BMD was noted for the entire study group (N = 9), after a mean duration of treatment of 14 +/- 1 months. The mean lumbar spine BMD Z score improved by 0.40 +/- 0.09 (P = 0.002) with alendronate therapy. The femoral neck BMD also increased by 4.5 +/- 1.4% per year with alendronate treatment (P = 0.013). The mean absolute gain in femoral neck BMD was 0.028 +/- 0.009 g/cm 2 (P = 0.013) for the study group (N = 9) after 14 +/- 1 months of therapy. The mean femoral neck BMD Z score improved 0.30 +/- 0.08 (P = 0.005) with treatment. BMD gains at the greater trochanter of 3.2 +/- 1.5% per year (P = 0.067) and at Ward's triangle of 9.1 +/- 4.2% per year (P = 0.061) were not statistically significant. Two patients discontinued alendronate treatment after 1 year because of epigastric or retrosternal pain. CONCLUSION: Oral alendronate treatment, given in combination with calcium supplementation and physiologic doses of vitamin D, resulted in significant improvements in lumbar spine and femoral neck BMD after a 14-month period in this small group of men with osteoporosis. Although controlled, prospective trials involving larger numbers of male patients with fracture incidence data are needed before definitive conclusions can be made, alendronate treatment seems to be effective in improving BMD in men with osteoporosis, similar to its efficacy in women.

Journal Article↗