Fear of COVID-19 as a precautionary measure to prevent the epidemic among the population of the Kurdistan Region/Iraq: based on a questionnaire survey.

Background and objectives: The World Health Organization (WHO) announced the appearance of a new coronavirus disease in Hubei province, China, to be a public health emergency of international concern. The objectives of this study can be highlighted through classifying the information sources for identifying protective practices, death probability, gender-death associations probability and education level. Methodology: This is a descriptive design study conducted among the Kurdistan Region/Iraq population via an online application between 1 March and 1 May 2020. Three hundred twenty people participated in this questionnaire study. The data were collected through an online form, relying upon a self-report questionnaire. The questionnaire had three main parts. The first part is related to the socio-demographic characteristics of the sample, including gender, age, family status, address status and education level. The second part involves the items related to precautionary measures using none, sometimes, and always. The last part contains items related to death probability owing to other causes and this includes five categories: extremely low, low, intermediate, high and extremely high. The validity and reliability of this questionnaire were revised by the panel of experts before the data collection. Results: The outcomes of the study revealed that the majority, ca. 73%, of the Kurdistan Region/Iraq population depended on TV to obtain information about COVID-19. Also, this investigation showed that there is a substantial association between participants with infection prevention and control practices relevant to COVID-19. Moreover, according to this study, there is a significant relationship between the death probability and COVID-19. Concurrently, there is not any significant association between other causes, namely cancer, heart diseases, diabetes and road traffic accidents, and the death probability. Conclusion: This study showed that for the majority of the Kurdistan Region/Iraq population the most reliable source of information for any COVID-19 related updates is the TV broadcast. This study also indicated that there is strong association for the majority of individuals regarding their practices for prevention from COVID-19 and death probability with COVID-19. However, there is not any substantial association between the epidemic and the other deadly calamities and the death probability.

Socioeconomic determinants and metabolic syndrome: Results from the Isfahan Healthy Heart Program.

Introduction: The prevalence of metabolic syndrome (MetS) is increasing in Iran. We assessed the relationship between socioeconomic status (SES) and Mets components in the Iranian population. MATERIALS AND METHODS: The sample for this study comprised a random cross-section of men and women from two province districts who participated in the Isfahan Healthy Heart Program (IHHP) in 2007. Each participant completed a questionnaire, underwent anthropometric testing and blood pressure measurements, and provided a blood sample. Mets was defined based on ATPIII criteria. Several SES dimensions, such as education, occupation, and number of children, as well as home, car, and personal computer ownership, were assessed to determine the participant's SES. RESULTS: A higher-than-average income, car ownership, owning or renting a private home, and having a computer are increasing towards increment in SES. All MetS components were more prevalent in participants defined as having a lower SES, while low HDL levels were more common in participants having an SES II (P>0.001). A multivariate analysis showed that having the lowest SES (I) increased the risk of MetS by 1.72 [1.44-2.07], whereas subjects having an SES III had a 1.23 [1.04-1.47] lower risk for MetS. CONCLUSIONS: The relationship between SES and Mets is due largely to behavioural factors, such as practicing unhealthy eating habits. Given the high prevalence of Mets in Iran, we propose that regular health check-ups may be useful in the early detection of the syndrome and, consequently, in the prevention of its effects. In addition, the early detection of MetS may result in the early diagnosis and prevention of cardiovascular diseases.

Could quality of life impact the prevalence of metabolic syndrome? Results from a population-based study of Swedish women: the Women's Health in the Lund Area Study.

BACKGROUND: The metabolic syndrome is regarded as an important risk factor for diabetes mellitus and cardiovascular disease. Metabolic syndrome could be associated with impaired quality of life (QoL). METHODS: The Women's Health in the Lund Area (WHILA) project covers 10,766 women born between December 2, 1935, and December 1, 1945, living in the Lund area, of Sweden by December 1, 1995. The primary objectives of this project were to survey perimenopausal women in this area and to evaluate their health status and lifestyles. We used the criteria for the metabolic syndrome, as defined by the National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III), which include three or more of five risk factors: central obesity, elevated serum triglycerides, low high-density lipoprotein cholesterol (HDL-C), and elevated blood pressure and fasting glucose. Analysis of most aspects of daily life and QoL according to the Gothenburg Quality of Life Instrument (GQL) was done. GQL refers to the WHO definition of health. RESULTS: A total number of 6913 (64.2%) women with a mean age (56.1) years fulfilled the criteria for screening procedure in the WHILA study. A positive association between women with metabolic syndrome and the following aspects of quality of life were found: "Partnership," "free time," "memory," and being "appreciated outside home." However, "economy," "health," "body image," and "fitness" had a negative association to the metabolic syndrome. CONCLUSION: QoL is an important factor for metabolic syndrome. Apart from traditional biological factors, prevention of metabolic syndrome should also encompass QoL.

Proghrelin-derived peptides influence the secretion of insulin, glucagon, pancreatic polypeptide and somatostatin: a study on isolated islets from mouse and rat pancreas.

Proghrelin, the precursor of the orexigenic and adipogenic peptide hormone ghrelin, is synthetized in endocrine (A-like) cells in the gastric mucosa. During its cellular processing, proghrelin gives rise to the 28-amino acid peptide desacyl ghrelin, which after octanoylation becomes active acyl ghrelin, and to the 23-amino acid peptide obestatin, claimed to be a physiological opponent of acyl ghrelin. This study examines the effects of the proghrelin products, alone and in combinations, on the secretion of insulin, glucagon, pancreatic polypeptide (PP) and somatostatin from isolated islets of mice and rats. Surprisingly, acyl ghrelin and obestatin had almost identical effects in that they stimulated the secretion of glucagon and inhibited that of PP and somatostatin from both mouse and rat islets. Obestatin inhibited insulin secretion more effectively than acyl ghrelin. In mouse islets, acyl ghrelin inhibited insulin secretion at low doses and stimulated at high. In rat islets, acyl ghrelin inhibited insulin secretion in a dose-dependent manner but the IC(50) for the acyl ghrelin-induced inhibition of insulin release was 7.5 x 10(-8) M, while the EC(50) and IC(50) values, with respect to stimulation of glucagon release and to inhibition of PP and somatostatin release, were in the 3 x 10(-12)-15 x 10(-12) M range. The corresponding EC(50) and IC(50) values for obestatin ranged from 5 x 10(-12) to 20 x 10(-12) M. Desacyl ghrelin per se did not affect islet hormone secretion. However, at a ten times higher concentration than acyl ghrelin (corresponding to the ratio of the two peptides in circulation), desacyl ghrelin abolished the effects of acyl ghrelin but not those of obestatin. Acyl ghrelin and obestatin affected the secretion of glucagon, PP and somatostatin at physiologically relevant concentrations; with obestatin this was the case also for insulin secretion. The combination of obestatin, acyl ghrelin and desacyl ghrelin in concentrations and proportions similar to those found in plasma resulted in effects that were indistinguishable from those induced by obestatin alone. From the data it seems that the effects of endogenous, circulating acyl ghrelin may be overshadowed by obestatin or blunted by desacyl ghrelin.

Pulses of somatostatin release are slightly delayed compared with insulin and antisynchronous to glucagon.

It was early proposed that somatostatin-producing delta-cells in pancreatic islets have local inhibitory effects on the release of insulin and glucagon. Recent observations that pulses of insulin and glucagon are antisynchronous make it important to examine the temporal characteristics of glucose-induced somatostatin release. Analysis of 30 s fractions from the perfused rat pancreas indicated that increase of glucose from 3 to 20 mmol/l results in initial suppression of somatostatin release followed by regular 4-5 min pulses. During continued exposure to 20 mmol/l glucose, the pulses of somatostatin overlapped those of insulin with a delay of 30 s. Somatostatin and glucagon pulses were coupled in antisynchronous fashion (phase shift 2.4+/-0.2 min), supporting the idea that the delta-cells have a local inhibitory effect on glucagon release. It was possible to remove the pulses of somatostatin and glucagon with maintenance of the insulin rhythmicity by addition of 1 micromol/l of the P2Y(1) receptor antagonist MRS 2179.

Expression of islet inducible nitric oxide synthase and inhibition of glucose-stimulated insulin release after long-term lipid infusion in the rat is counteracted by PACAP27.

Chronic exposure of pancreatic islets to elevated plasma lipids (lipotoxicity) can lead to beta-cell dysfunction, with overtime becoming irreversible. We examined, by confocal microscopy and biochemistry, whether the expression of islet inducible nitric oxide synthase (iNOS) and the concomitant inhibition of glucose-stimulated insulin release seen after lipid infusion in rats was modulated by the islet neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP)27. Lipid infusion for 8 days induced a strong expression of islet iNOS, which was mainly confined to beta-cells and was still evident after incubating islets at 8.3 mmol/l glucose. This was accompanied by a high iNOS-derived NO generation, a decreased insulin release, and increased cyclic GMP accumulation. No iNOS expression was found in control islets. Addition of PACAP27 to incubated islets from lipid-infused rats resulted in loss of iNOS protein expression, increased cyclic AMP, decreased cyclic GMP, and suppression of the activities of neuronal constitutive (nc)NOS and iNOS and increased glucose-stimulated insulin response. These effects were reversed by the PKA inhibitor H-89. The suppression of islet iNOS expression induced by PACAP27 was not affected by the proteasome inhibitor MG-132, which by itself induced the loss of iNOS protein, making a direct proteasomal involvement less likely. Our results suggest that PACAP27 through its cyclic AMP- and PKA-stimulating capacity strongly suppresses not only ncNOS but, importantly, also the lipid-induced stimulation of iNOS expression, possibly by a nonproteasomal mechanism. Thus PACAP27 restores the impairment of glucose-stimulated insulin release and additionally might induce cytoprotection against deleterious actions of iNOS-derived NO in beta-cells.

Glucose induces glucagon release pulses antisynchronous with insulin and sensitive to purinoceptor inhibition.

Both increase of the glucose concentration and activation of purinoceptors are known to affect pancreatic alpha-cells. Effects obtained with various purino derivatives at 2.8 and 8.3 mmol/liter glucose have been taken to indicate that external ATP is less potent than adenosine as a stimulator of glucagon release. However, when making a corresponding comparison at 20 mmol/liter glucose, we observed marked stimulation of glucagon release from isolated rat islets with 100 micromol/liter adenosine-5-O-2-thiodiphosphate but inhibition with 10 micromol/liter adenosine. Analyses of 30-sec samples of perfusate from rat pancreas indicated that a rise of the glucose concentration from 3 to 20 mmol/liter rapidly induces a glucagon peak followed by regular 4- to 5-min pulses. The glucagon pulses preceded those of insulin with a phase shift (1.8 +/- 0.1 min) near half the interpeak interval. Because of the antisynchrony, the maximal glucagon effect on liver cells will be manifested during periods with low concentrations of insulin. In support for the idea that neural P2Y(1) receptors are important for coordinating the secretory activity of the islets, both the insulin and glucagon pulses disappeared in the presence of the purinoceptor inhibitor MRS 2179 (10 micromol/liter). However, in contrast to what was observed for insulin, MRS 2179 lowered average glucagon release to the level of the oscillatory nadirs.

Selective induction of inducible nitric oxide synthase in pancreatic islet of rat after an intravenous glucose or intralipid challenge.

OBJECTIVE: Constant exposure of pancreatic islets to high levels of glucose or free fatty acids can lead to irreversible beta-cell dysfunction, a process referred to as glucotoxicity or lipotoxicity, respectively. In this context a role for nitric oxide generated by pancreatic islet has been suggested. The present investigation examined whether the route of glucose administration, i.e., given orally (OG) or infused intravenously (IVG), could have any effect on the expression and activity of inducible nitric oxide synthase (iNOS) in pancreatic islets. METHODS: Rats were infused with glucose (50%) or Intralipid intravenously for 24 h or given glucose orally. A freely fed control group (FF) was also included. At 24 h rats were killed and blood samples were drawn for analysis of plasma insulin, glucagon, and glucose. Pancreatic islets were harvested from each animal and investigated for the occurrence of iNOS by the use of confocal microscopy, western blot, and high-performance liquid chromatographic analysis. The effect of intravenously infused glucose was then compared with the effect of an intravenous infusion of Intralipid (IL). RESULTS: Plasma insulin levels were markedly decreased after 24 h of infusion of glucose (IVG group) or Intralipid (IL group) compared with the FF or OG group. Plasma glucagon and glucose levels were markedly increased in the IVG group, whereas both parameters were decreased in the IL group. No significant differences in plasma insulin, glucagon, or glucose were found between the OG and FF groups. Immunocytochemical (confocal microscopy), western blot, and biochemical (high-performance liquid chromatographic) analyses showed that a sustained increase in plasma level of glucose or free fatty acids by an intravenous infusion of either nutrient for 24 h resulted in a marked expression and activity of iNOS in pancreatic islets. No sign of iNOS expression could, however, be detected in the islets of FF control or OG rats. CONCLUSION: The data suggest that impaired beta-cell function found after 24 h of an intravenous infusion of glucose or Intralipid might be mediated, at least in part, by the induction of iNOS in pancreatic islets. This may subsequently result in an exclusive production of nitric oxide, which is deleterious for beta-cells.

Long-term infusion of nutrients (total parenteral nutrition) suppresses circulating ghrelin in food-deprived rats.

BACKGROUND: Ghrelin derives from endocrine cells (A-like cells) in the stomach (mainly the oxyntic mucosa). Its concentration in the circulation increases during fasting and decreases upon re-feeding. This has fostered the notion that the absence of food in the upper gastrointestinal (GI) tract stimulates the secretion of ghrelin. The purpose of the present study was to determine the concentration of ghrelin in serum and oxyntic mucosa after replacing food with intravenous (iv) infusion of nutrients for 8 days using the technique known as total parenteral nutrition (TPN) MATERIALS AND METHODS: Male Sprague-Dawley rats (200-250 g) were given nutrients (lipids, glucose, amino acids, minerals and vitamins) by iv infusion for 8 days during which time they were deprived of food and water; another group was deprived of food for 24-48 h (fasted controls), while fed controls had free access to food and water. Serum ghrelin, gastrin and pancreastatin concentrations were measured together with the ghrelin content of the oxyntic mucosa. Plasma insulin and glucose as well as serum lipid concentrations were also determined. RESULTS: Fasted rats had higher serum ghrelin than TPN rats and fed controls. The oxyntic mucosal ghrelin concentration (and content) was lower in TPN rats than in fasted rats or fed controls. The serum gastrin and pancreastatin concentrations were lower in TPN rats and fasted rats than in fed controls. The plasma insulin concentration was 87 pmol/l+/-8 (SEM) in TPN rats compared to 101+/-16 pmol/l in fed controls; it was 26+/-14 pmol/l in fasted rats. The basal plasma glucose level was 11+/-0.6 mmol/l in TPN rats and 12+/-0.8 mmol/l in fed controls; it was 7+/-0.3 mmol/l in fasted rats. In TPN rats, the serum concentrations of free fatty acids, triglycerides and cholesterol were increased by 100%, 50% and 25%, respectively, compared to fed controls. Fasted rats had higher circulating concentrations of free fatty acids (20%) and lower concentrations of triglycerides (-40%) than fed controls; fasted rats did not differ from fed controls with respect to serum cholesterol. CONCLUSION: The circulating ghrelin concentration is high in situations of nutritional deficiency (starvation) and low in situations of nutritional plenty (free access to food or TPN). The actual presence or absence of food in the GI tract seems irrelevant. Circulating insulin and glucose concentrations did not differ much between TPN rats and fed controls; serum lipids, however, were elevated in the TPN rats. We suggest that elevated blood lipid levels contribute to the suppression of circulating ghrelin in rats subjected to TPN for 8 days.

Inhibition of purinoceptors amplifies glucose-stimulated insulin release with removal of its pulsatility.

External ATP has been proposed to be an autocrine regulator of glucose-stimulated insulin secretion and responsible for the synchronization of the Ca2+ rhythmicity in the beta-cells required for a pulsatile release of insulin from the pancreas. The importance of external ATP for glucose-stimulated insulin release was evaluated in rats with the aid of 2-deoxy-N-methyladenosine-3,5-bisphosphate (MRS 2179), an inhibitor of the purinoceptors known to affect the Ca2+ signaling in beta-cells. The concentration of cytoplasmic Ca2+ was measured in single beta-cells and small aggregates with ratiometric fura-2 technique and the release of insulin recorded from isolated islets and the perfused pancreas. Addition of 1 micromol/l ATP induced premature cytoplasmic Ca2+ concentration ([Ca2+]i) oscillations similar to those found in beta-cells exposed to 20 mmol/l glucose. In most experiments, the presence of 10 micromol/l MRS 2179 did not remove the glucose-induced [Ca2+]i rhythmicity in single beta-cells or the synchronization seen in coupled cells. Nevertheless, the same concentration of MRS 2179 promptly interrupted the pulsatility (frequency 0.22 +/- 0.01/min) of insulin secretion, raising the total amounts released from the pancreas. Prolonged exposure of islets to 1 and 10 micromol/l MRS 2179 enhanced insulin secretion at 20 mmol/l glucose 33% (P < 0.05) and 63% (P < 0.01), respectively, without affecting the release at 3 mmol/l glucose. The results support the idea that neural ATP signals entrain the islets into a common rhythm resulting in pulsatile release of insulin and that glucose stimulation of the secretory activity is counteracted by accumulation of inhibitory ATP around the beta-cells.

Effects of total parenteral nutrition on rat enteric nervous system, intestinal morphology, and motility.

Total parenteral nutrition (TPN) is often crucial for patients not being able to feed enterally or having intestinal absorptive deficits. Enteral nutrition is, however, frequently regarded vital for maintaining functional and structural intestinal integrity. The aim of this study was to investigate possible effects of TPN on rat distal small intestine compared to enterally fed identically housed controls, regarding the enteric nervous system (ENS), motility in vitro, and morphology. This study shows that motor responses evoked by electrical stimulation or exposure to vasoactive intestinal peptide (VIP), pituitary adenylate cyclase activating peptide-27 (PACAP-27), and nitric oxide (NO) donor were unchanged. By using immunohistochemistry, the numbers of submucous (P < 0.05) and myenteric (P < 0.05) nerve cells were found to increase, expressed as numbers per unit length. The percentage of neurons expressing VIP, PACAP-27, NO-synthase, and galanin remained unchanged, however. By in situ hybridization the number of submucous neurons expressing neuropeptide Y-mRNA was found to decrease (P < 0.05); the other populations were unaltered. Morphometry revealed an increased submucosal thickness (P < 0.05), while intestinal circumference markedly decreased (P < 0.0001) in TPN-treated rats. In conclusion, TPN treatment resulted in reduced intestinal circumference leading to condensation of enteric neurons. No marked changes in neurotransmitter expression of the enteric neurons or in motor activity were noted.

Ghrelin activates neuronal constitutive nitric oxide synthase in pancreatic islet cells while inhibiting insulin release and stimulating glucagon release.

In view of our previous data, showing that ghrelin and nitric oxide (NO) display apparently parallel effects on insulin secretion (inhibitory) and glucagon secretion (stimulatory), we have now investigated the effect of ghrelin on islet hormone secretion in relation to its effect on NO synthase (NOS) isoenzymes in isolated rat pancreatic islets. Dose-response studies revealed that ghrelin at concentrations of 0.01-1 micromol l-1 inhibited insulin secretion stimulated by 8.3 mmol l-1 glucose, while ghrelin at concentrations lower than the physiological range (0.01 pmol l-1 to 1 nmol l-1) were without effect. In contrast, glucagon secretion was stimulated by 1.0 nmol l-1 to 1 micromol l-1 ghrelin. These effects of ghrelin on insulin and glucagon secretion were accompanied by increased NO production through activation of neuronal constitutive NOS (ncNOS). Ghrelin had no appreciable effect on the activity of inducible NOS (iNOS) in the islets. Addition of an NO scavenger (cPTIO) or the NOS inhibitor L-NAME to the incubation medium prevented the effects of ghrelin on hormone secretion from isolated islets. The present results confirm our previous data showing that ghrelin inhibits insulin and stimulates glucagon secretion from pancreatic islets of the mouse and we now show similar effects in rat islets. The effects of ghrelin were accompanied by an increased rate of NO production. Conceivably, ncNOS activation partly accounts for to the inhibitory effect of ghrelin on insulin secretion and the stimulatory effect of ghrelin on glucagon secretion.

Defective insulin secretion during total parenteral nutrition in rat and its normalization by pituitary adenylate cyclase-activating polypeptide 27.

The role of PACAP27, PACAP38 and VIP in the regulation of insulin release from pancreatic islets isolated from rats previously subjected to total parenteral nutrition (TPN) for 10 days was studied. Glucose-stimulated insulin secretion from islets of TPN rats was attenuated in parallel with cyclic AMP production. Immunocytochemistry showed an increased number of VIP-immunoreactive nerve fibers in the pancreatic islets of TPN rats. PACAP27, PACAP38 and VIP dose dependently and to the same magnitude potentiated insulin secretion from the islets of freely fed controls in the presence of a substimulatory glucose concentration (8.3 mmol/l). The secretory response of islets from TPN-treated rats to these neuropeptides was, however, markedly exaggerated compared to the controls. The insulin response of islets from TPN-treated rats to PACAP27 and PACAP38 was much greater than to VIP. With respect to insulin secretion, TPN treatment shifted the PACAP27 and PACAP38 dose-response curve to the left by two orders of magnitude. In the presence of 8.3 mmol/l glucose, cAMP accumulation was slightly higher in islets from TPN rats and the PACAP27, PACAP38 and VIP-stimulated increase in the cAMP production was markedly greater compared to the controls. Additional complementary in vivo experiments showed that PACAP27 normalized the defective glucose-stimulated insulin secretory response of TPN-treated rats. The data suggest that the defective nutrient-stimulated insulin secretion seen after long-term TPN treatment could be normalized by agents stimulating cAMP production possibly through cAMP/PK A-pathway.

Acute pancreatitis, expression of inducible nitric oxide synthase and defective insulin secretion.

A high level of nitric oxide (NO) produced by inducible NO synthase (iNOS) is involved in pancreatic beta-cell dysfunction and apoptosis. In the present study, we examined whether iNOS is also expressed in beta cells after induction of acute pancreatitis (AP) in the rat. Pancreatic islets taken from AP animals and incubated for 60 min in the presence of 20.0 mmol/l glucose showed a decreased insulin secretory response to glucose. The basal insulin release at 1.0 mmol/l glucose was also moderately reduced. Experiments on the dynamics of insulin secretion from perfused pancreas revealed an impairment of both first and second phase of glucose-stimulated insulin release after the induction of AP. Confocal microscopy demonstrated that most of the beta cells in pancreas of rat with AP expressed strong immunoreactivity for iNOS. This was further confirmed by biochemical and Western blot analysis that showed a marked increase in iNOS protein expression and enzyme activity concomitant with a modest reduction in the cNOS protein and activity. Although the mechanisms underlying the defective insulin secretory response of beta cells seen during the early stage of AP are complex, the present finding suggests that the expression of iNOS and a marked iNOS-derived NO production in the beta cells may play at least a contributory role in the impairment of beta-cell function.