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Jamal Golbahar,1,2,* Maha Al-Ayadhi,2,* Negalla Mohan Das,2 Khalid Gumaa,2 1Department of Molecular Medicine, Al-Jawhara Centre for Genetic Diagnosis and Research, 2Department of Medical Biochemistry, College of Medicine and Medical Sciences, AGU, Manama, Bahrain *These authors contributed equally to this articleBackground: In women with polycystic ovary syndrome (PCOS), despite a high prevalence of insulin resistance, hyperandrogenemia, and disturbances in the secretion of gonadotrophin, the principal causes of biochemical abnormalities and the best endocrine markers for PCOS have not been fully identified.Subjects and methods: Serum levels of insulin, glucose, follicle-stimulating hormone (FSH), luteinizing hormone (LH), total testosterone, estrogen, sex hormone-binding capacity (SHBG), and other related indices such as homeostasis model assessment, insulin glucose ratios, LH/FSH ratios, and the free androgen index (FAI) were determined and compared in women with PCOS (n = 50) and women without PCOS (n = 50).Results: In multivariate logistic regression analyses, among all insulin resistance indices, only hyperinsulinemia (odds ratio [OR] = 2.6; confidence interval [CI]: 1.3–5.2; P = 0.008) was significantly and independently associated with PCOS when adjusted for body mass index (BMI), hyperandrogenemia, and LH/FSH ratios. The LH/FSH ratio (OR = 5.4; CI: 1.2–23.0, P = 0.03) was the only marker among those indices for inappropriate gonadotrophin secretion that significantly and independently associated with PCOS when adjusted for BMI and hyperinsulinemia. Among those indices for hyperandrogenemia, FAI (OR = 1.1; CI: 1.0–2.7; P = 0.02) and SHBG (OR = 1.2; CI: 1.2–3.4; P = 0.03) were significantly and independently associated with PCOS when adjusted for BMI and hyperinsulinemia. In addition, receiver operating characteristic analysis showed that the best predictive markers for PCOS were insulin (area under the curve [AUC] = 0.944; CI: 0.887–0.989), FAI (AUC = 0.932; CI: 0.895–0.993), SHBG (AUC = 0.924; CI: 0.87–0.978), and LH/FSH ratios (AUC = 0.906; CI: 0.821–0.965).Conclusion: For insulin and LH/FSH ratios, FAI, and SHBG seemed the best predictors and markers for insulin resistance, inappropriate gonadotrophin secretion, and hyperandrogenemia, respectively, with high sensitivity and specificity for identifying Bahraini women with and without PCOS.Keywords: polycystic ovary syndrome, insulin resistance, gonadotrophin, hyperandrogenemia, diagnostic markers

1. Fluid intake, urine output and evaporative water loss were measured and fluid balance calculated in sixteen subjects for 1 d before Ramadan, during weeks 1???5 of fasting and on the 10th day after the end of Ramadan.2. Plasma osmolality at 06.00 hours, the beginning of the fast, at 18.00 hours, before breaking the fast and at 19.00 hours, 1 h after breaking the fast, and urine osmolality during the day and night were measured before, during and after Ramadan.3. All subjects developed an initial negative fluid balance which was maximum at the beginning of week 3 of fasting and that deficit was compensated for during the later weeks.4. Compensation was brought about by an increase in urine concentration, a decrease in urine volume by day, and salt retention.5. No significant changes were observed in plasma osmolality during the days of fasting and the ???setting??? of plasma osmolality during Ramadan also was not changed.6. It was concluded that healthy young adults maintain good control of fluid and electroytes during Ramadan. [ABSTRACT FROM PUBLISHER]

1. The changes in serum levels of uric acid and lipids during 1 month of starvation-refeeding were measured in sixteen male volunteers.2. Uric acid levels increased linearly with the duration of the experiment. The increase was positively correlated with the increase in serum triglycerides but not with cholesterol or phospholipids.3. Triglycerides increased at a faster rate than uric acid implying that the increase in uric acid was secondary to that of the lipid.4. It was concluded that the purine and lipid synthetic pathways are linked through a common small-molecular-weight effector rather than through the sharing of a common enzyme. [ABSTRACT FROM PUBLISHER]

We have previously reported that infection with Plasmodium yoelii, Plasmodium chabaudi, or injection of extracts from malaria-parasitized red blood cells induces hypoglycemia in normal mice and normalizes the hyperglycemia in streptozotocin (STZ)-diabetic mice. P yoelii glycosylphosphatidylinositols (GPIs) were extracted in chloroform:methanol:water (CMW) (10:10:3), purified by high-performance thin layer chromatography (HPTLC) and tested for their insulin-mimetic activities. The effects of P yoelii GPIs on blood glucose were investigated in insulin-resistant C57BL/ks-db/db diabetic mice. A single intravenous injection of GPIs (9 and 30 nmol/mouse) induced a significant dose-related decrease in blood glucose (P < .001), but insignificantly increased plasma insulin concentrations. A single oral dose of 2.7 micromol GPIs per db/db mouse significantly lowered blood glucose (P < .01). P yoelii GPIs in vitro (0.062 to 1 micromol/L) significantly stimulated lipogenesis in rat adipocytes in a dose-dependent manner both in the presence and absence of 10(-8) mol/L insulin (P < .01). P yoelii GPIs stimulated pyruvate dehydrogenase phosphatase (PDH-Pase) and inhibited both cyclic adenosine monophosphate (cAMP)-dependent protein kinase A and glucose-6-phosphatase (G6Pase). P yoelii GPIs had no effect on the activity of the gluconeogenic enzymes fructose-1,6-bisphosphatase (FBPase) and phosphoenolpyruvate carboxykinase (PEPCK). This is the first report of the hypoglycemic effect of P yoelii GPIs in murine models of type 2 diabetes. In conclusion, P yoelii GPIs demonstrated acute antidiabetic effects in db/db mice and in vitro. We suggest that P yoelii GPIs, when fully characterized, may provide structural information for the synthesis of new drugs for the management of diabetes., (Copyright 2004 Elsevier Inc.)

We have previously shown that infection with Plasmodium yoelii malaria or injection of extracts from malaria-parasitized red cells induces hypoglycemia in normal mice and normalizes the hyperglycemia in mice made moderately diabetic with streptozotocin. Inositol phosphoglycans (IPGs) are released outside cells by hydrolysis of membrane-bound glycosylphosphatidylinositols (GPIs), and act as second messengers mediating insulin action. The C57BL/Ks-db/db and C57BL/6J-ob/ob mice offer good models for studies on human obesity and Type 2 diabetes. In the present study, we show that a single iv injection of IPG-A or IPG-P extracted from P. yoelii significantly (P < 0.02) lowers the blood glucose in STZ-diabetic, db/db, and in ob/ob mice for at least 4--6 h. Using rat white adipocytes, IPG-P increased lipogenesis by 20--30% in the presence and absence of maximal concentrations of insulin (10(-8) M) (P < 0.01) and stimulated pyruvate dehydrogenase (PDH) phosphatase in a dose-related manner. Both IPG-A and IPG-P inhibited c-AMP-dependent protein kinase (PKA) in a dose-related manner. Compositional analysis of IPGs after 24 h hydrolysis revealed the presence of myo-inositol, phosphorus, galactosamine, glucosamine, and glucose in both IPG-A and IPG-P. However, hydrolysis of IPGs for 4 h highlighted differences between IPG-A and IPG-P. There are some functional similarities between P. yoelii IPGs and those previously described for mammalian liver. However, this is the first report of the hypoglycemic effect of IPGs in murine models of Type 2 diabetes. We suggest that IPGs isolated from P. yoelii, when fully characterized, may provide structural information for the synthesis of new drugs for the management of diabetes mellitus., (Copyright 2001 Academic Press.)

Rat diaphragm showed a nine to ten-fold increase in the dry and wet weights and a four-fold increase in its surface area between 21 and 540 days of age. The increase was the most rapid between days 21 and 90, thereafter a non-significant trend of increase was maintained at least up to 360 days of age followed by a tendency to decrease. The total collagen content of the diaphragm paralleled the increase in surface area with progressing age. The collagen content significantly dropped when expressed relative to the dry weight of the diaphragm, between 21 and 90 days of age. This trend was maintained till 180 days of age but thereafter significantly rise was seen. These later changes may be due to elenated synthesis and/or reduced degradation of collagen, and may contribute to the decline in contractility of the diaphragm as age advances.

Severe asthma and diabetes have been reported not to co-exist in the same patient. Various studies have attributed this to the possible association of asthma with hyperinsulinism, increased responsiveness to insulin or to beta-blockade. Previous studies have not addressed all these possible mechanisms in the same patient. In this prospective study, 7 atopic asthmatics and 7 age and sex-matched healthy controls underwent glucose, insulin and glucagon tolerance tests. The results showed no evidence of hyperinsulinism or increased responsiveness to insulin. Intravenous administration of glucagon, however, showed a lesser increase of glucose and insulin in asthmatics. Since glucagon has a beta-agonist effect on the liver and activates glycogenolysis and gluconeogenesis via beta-receptor stimulation and stimulates insulin secretion by activating adenylate cyclase of pancreatic beta-cells through beta-receptors, the results of glucagon tolerance test in our study may therefore suggest the presence of partial beta-blockade in atopic asthmatics.

1. Diaphragms from BIO 14.6 dystrophic hamsters had lower dry weights and higher collagen content than did controls, BIO F1B. 2. The increase in pepsin-solubilized collagen affected mainly types III and V, and there was a concomitant decrease in the beta and high molecular weight (HMW) collagen aggregates. 3. These findings are similar to the observations in myotonia congenita and imply that the dystrophic process increases collagen synthesis. 4. In addition, there is possibly a genetic mutation of amino acids at points of contact of collagen monomers. 5. Alternatively, there may be reduced hydroxylation of lysine residues and hence in the degree of glycosylation of collagen resulting in decreased cross-linking and aggregation.

The diagnosis of recurrent hereditary polyserositis (RHP; also known as familial Mediterranean fever) remains one of exclusion since there has been no specific diagnostic laboratory test. A previous study suggested that the disorder is related to abnormal catecholamine metabolism. Plasma dopamine beta-hydroxylase (DBH) activity was assayed spectrophotometrically in 91 RHP patients and 162 controls. The activity was significantly higher in untreated symptom-free patients and in patients with acute attacks, than in controls (mean [SEM] 155.8 [14.1] vs 43.3 [1.9] mumol/min/1 p less than 0.0001). Colchicine treatment reduced DBH activity to control levels. The test showed a high diagnostic accuracy and specificity for RHP, whether the patient was symptom-free or having an acute attack. Moreover, it is easy to carry out.

A blood glucose lowering extract of a mixture of five plants in use by Kuwaiti diabetics was studied for the identification of its active component(s). Only the extracts of myrrh and aloe gums effectively increased glucose tolerance in both normal and diabetic rats. The remaining components, gum olibanum, Nigella sativa seeds and gum assafoetida were without effect.

Little is known of the blood sugar regulation in the camel and the morphology and function of its endocrine pancreas. The present paper describes the light microscopic structure and hormone content of the endocrine pancreas of the one-humped camel. Staining of pancreatic sections with haematoxylin-eosin or aldehyde-fuchsin showed numerous islets evenly distributed in all parts of the pancreas. Immunocytochemical staining for insulin or glucagon indicated that islets were predominantly composed of centrally located B-cells, surrounded by a peripheral rim of A-cells. Corresponding stainings for somatostatin or pancreatic polypeptide (PP) demonstrated that D-cells comprised only a small part of the islet volume while PP-cells were common both within and outside the islets. There were no obvious differences between the frequency of the various islet cells in different pancreatic regions. The pancreatic hormone concentrations roughly corresponded to the frequency of the different islet cell types. Insulin appeared most abundant followed by glucagon, PP and somatostatin in decreasing order. The concentrations of each of the hormones were similar in different regions of the gland. It is concluded that the endocrine pancreas of the one-humped camel is dispersed into islets of the same size and cellular composition as has been described in many other mammalian species.

The mechanism of the inhibitory effect of steroid hormones, progesterone and prednisolone on the incorporation of [3H]-thymidine into pancreatic islet cell DNA was investigated. Treatment with either hormone had no effect on the incorporation of 32P-orthophosphate into islet cell DNA. Both prednisolone (10 microM) and progesterone (3 microM) markedly stimulated the activity of the enzyme thymidylate synthetase of islet cells possibly leading to increased synthesis of endogenous thymidine which resulted in dilution of the [3H]-thymidine added to the islets in tissue culture. Prednisolone (10 microM) significantly increased both insulin biosynthesis and release, while at 5 microM it was effective in increasing only insulin release. In contrast, progesterone at the two concentrations employed did not affect insulin biosynthesis or release. The smaller doses of both hormones markedly stimulated the total protein biosynthesis.

Activities of the cysteine proteinases cathepsins B and H and of the chymotrypsin-like cathepsin G were determined in amniotic fluid of rats during the last third of gestation. Activities of cathepsins B and G were found to significantly increase with increasing gestational age while cathepsin H activity decreased. It was concluded that cathepsins may participate in the destabilization of fetal membranes and therefore may contribute to their rupture.

Natural human interleukin and the recombinant human IL-1 alpha and beta isomers were tested for effects on both fetal and adult rat isolated pancreatic islets. IL-1 alpha inhibited both replication and insulin secretion and decreased the insulin content of both islets. In contrast, the beta isomer did not affect fetal islets. It is concluded that the two isomers may have different avidities for the same receptors, or that receptors are expressed at different stages of differentiation.