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Biomedical subjects

G van Dijk

Publications and source records attributed to G van Dijk.

At least 19 recordsLinked to original sources

Agouti-related protein prevents self-starvation.

Food restriction leads to a paradoxical increase in physical activity and further suppression of food intake, such as observed in anorexia nervosa.(1,2) To understand this pathophysiological process, we induced physical hyperactivity and self-starvation in rats by restricting food in the presence of running wheels. Normally, decreased melanocortin receptor activity will prevent starvation.(3,4) However, we found that self-starvation increased melanocortin receptors in the ventral medial hypothalamus, a brain region involved in eating behavior.(5) Suppression of melanocortin receptor activity, via central infusion of Agouti-related protein (AgRP), increased survival rate in these rats by counteracting physical hyperactivity, food intake suppression as well as deregulated body temperature. We conclude that self-starvation may result from insufficient suppression of central melanocortin receptor activity.

Agouti-Related Protein↗

[Design of custom-shaped abutments for single-tooth crowns on implants].

Single-tooth implants have become a predictable treatment option. Acceptable esthetics are an important factor for success. The emergence profile of the crown in the cervical region is complicated by the discrepancy between the round shape and the small diameter of the implant and the desired anatomical shape of the crown. An abutment on an implant has to provide this natural looking emergence profile and has to support the crown. Custom-shaped abutments are the best option for this task. Many items influence the design. This article discusses a set of guidelines for the design of custom-shaped abutments for single-tooth implants.

Crowns↗

Dopamine mediation of the feeding response to violations of spatial and temporal expectancies.

The present studies were aimed at further characterizing the role of DA in motivation. Rats, conditioned to expect food in one environment and no food in another, all received food on the test night. Those in the environment in which food was unexpected ate four times as much as those eating where food was expected. The overeating was eliminated by administration of the D2 antagonist raclopride. Another expectancy, timing of light offset in rats entrained to a fixed light--dark cycle, was violated by unexpectedly turning the lights off 1 h early. This provoked an elevation in food intake, which was also eliminated by the administration of raclopride. Feeding in two other situations not involving violation of expectancies (food deprivation; normal light offset) was unaffected by DA antagonism. These findings support the idea that DA signals errors in expectancy and that DA signaling is necessary for certain behavioral responses to unexpected events.

Animals↗

Hypothalamic, metabolic, and behavioral responses to pharmacological inhibition of CNS melanocortin signaling in rats.

The CNS melanocortin (MC) system is implicated as a mediator of the central effects of leptin, and reduced activity of the CNS MC system promotes obesity in both rodents and humans. Because activation of CNS MC receptors has direct effects on autonomic outflow and metabolism, we hypothesized that food intake-independent mechanisms contribute to development of obesity induced by pharmacological blockade of MC receptors in the brain and that changes in hypothalamic neuropeptidergic systems known to regulate weight gain [i.e., corticotropin-releasing hormone (CRH), cocaine-amphetamine-related transcript (CART), proopiomelanocortin (POMC), and neuropeptide Y (NPY)] would trigger this effect. Relative to vehicle-treated controls, third intracerebroventricular (i3vt) administration of the MC receptor antagonist SHU9119 to rats for 11 d doubled food and water intake (toward the end of treatment) and increased body weight ( approximately 14%) and fat content ( approximately 90%), hepatic glycogen content ( approximately 40%), and plasma levels of cholesterol ( approximately 48%), insulin ( approximately 259%), glucagon ( approximately 80%), and leptin ( approximately 490%), whereas spontaneous locomotor activity and body temperature were reduced. Pair-feeding of i3vt SHU9119-treated animals to i3vt vehicle-treated controls normalized plasma levels of insulin, glucagon, and hepatic glycogen content, but only partially reversed the elevations of plasma cholesterol ( approximately 31%) and leptin ( approximately 104%) and body fat content ( approximately 27%). Reductions in body temperature and locomotor activity induced by i3vt SHU9119 were not reversed by pair feeding, but rather were more pronounced. None of the effects found can be explained by peripheral action of the compound. The obesity effects occurred despite a lack in neuropeptide expression responses in the neuroanatomical range selected across the arcuate (i.e., CART, POMC, and NPY) and paraventricular (i.e., CRH) hypothalamus. The results indicate that reduced activity of the CNS MC pathway promotes fat deposition via both food intake-dependent and -independent mechanisms.

Animals↗

Behavioral and physiological responses to stress are affected by high-fat feeding in male rats.

Interactions between monoaminergic neurochemistry and macronutrient intake have been frequently shown. Because monoaminergic systems in the brain are also closely involved in behavioral and physiological stress responses it can be hypothesized that differences in the macronutrient composition of diets are reflected in these responses. The present studies, therefore, were designed to assess the consequences of a change in dietary macronutrient composition on a variety of physiological and behavioral responses (both acute and long-term) to a number of stressors. The effect of chronic high-fat (HF; 61% kcal from fat) feeding on the stress responses was compared with controls receiving regular high-carbohydrate (HC; 63% kcal from carbohydrates) laboratory chow. Rats were kept on this diet for at least 2 months before they were exposed to either psychological (social defeat) or physiological (lipopolysaccharide, LPS, administration) stress. At baseline, chronic HF feeding caused a slight, but significantly reduction in body temperature relative to that observed in HC-fed rats. Following social defeat or LPS injection, HF feeding caused a faster recovery of the body temperature increase relative to animals on the HC diet. Stress-induced suppression of home cage locomotor activity and body weight gain were also reduced by HF feeding. The serotonergic 5-HT(1a) receptor hyposensitivity that was observed in HC-fed rats 2 weeks after stress was absent in the HF regimen. Although the present results cannot be readily interpreted as showing purely beneficial effects of high-fat diets on stress responsivity, the findings in the present study do encourage further investigation of possible ameliorating effects of high-fat diets on aspects of the behavioral and physiological response stress.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

The role of leptin in the regulation of energy balance and adiposity.

Since its discovery, leptin (a 167-amino acid product of the OB gene) has quickly moved to the forefront as an important hormone for regulation of energy balance. It closes a feedback loop from adipose tissue to hypothalamic neuropeptide-containing neural circuitry involved in regulation of food intake and neuroendocrine/autonomic outflow. While increased central leptin signalling reduces adiposity via a reduction in food intake, it also has remarkable metabolic effects that promote leanness, independent of food intake. These include: (i) increased energy expenditure, (ii) in-place degradation of fat, and (iii) increased thermogenesis. Hypothalamic neurones that synthesize corticotropin releasing hormone and melanocortins (i.e. alpha-melanocyte-stimulating hormone and agouti-related protein) are likely effector pathways that mediate the anorexigenic and metabolic effects of leptin. Activation of sympathetic outflow (via neuropeptidergic effector pathways of central leptin) to a number of tissues that store fat might be an important mechanism through which these peripheral metabolic effects are elicited. It is proposed that these peripheral metabolic effects contribute to the satiating properties of leptin.

Adipose Tissue↗

Prevalence and association between herpes simplex virus types 1 and 2-specific antibodies in attendees at a sexually transmitted disease clinic.

BACKGROUND: Seroprevalence of herpes simplex virus type 1 (HSV-1) and HSV-2 was determined in 1993 and 1998 in a randomly selected study group of 1024 and 654 attendees, respectively, at the sexually transmitted disease (STD) clinic of the University Hospital Rotterdam-Dijkzigt, The Netherlands. Correlations of HSV-1 and HSV-2 seropositivity were investigated. The relationship between HSV-1 and HSV-2 antibodies was also studied. METHODS: Data were collected in a cross-sectional study from February 1993 until February 1994 and from January 1998 until December 1998. Glycoprotein G (gG) HSV type specific serum IgG was determined. RESULTS: Seroprevalence of HSV-1 was 68% versus 59% (1993 versus 1998, chi(2)-test P < 0.001), of HSV-2 it was 30% versus 22% (1993 versus 1998, chi(2)-test P < 0.001). Using logistic regression analyses, HSV-1 and HSV-2 seropositivity were significantly associated with age and ethnicity in both groups. In 1993, HSV-1 seropositivity also correlated with lower level of education and female gender, whereas in 1998 it correlated with 'number of sexual partners in the past 6 months' and 'present diagnosis of STD'. In both groups, HSV-2 seropositivity was also more prevalent in females and related to sexual lifestyle variables. In an exposure-disease model, HSV-1 seropositivity was not correlated with HSV-2 seropositivity (odds ratio 1993 = 1.1, 95% CI : 0.8--1.7; odds ratio in 1998 = 1.0, 95% CI : 0.5--1.8). CONCLUSIONS: Seroprevalence of HSV-1 and HSV-2 is falling among STD clinic attendees in Rotterdam. A changing pattern of risk factors for HSV-1 seropositivity indicates increasing sexual transmission of HSV-1. Seropositivity for HSV-2 correlated with known risk factors. A previous HSV-1 infection does not reduce susceptibility to subsequent genital HSV-2 infections.

Adolescent↗

Ethanol-induced c-fos expression in catecholamine- and neuropeptide Y-producing neurons in rat brainstem.

BACKGROUND: Previous studies have used c-Fos-like immunoreactivity (cFLI) to examine the neuroanatomical location of cells that are activated in response to ethanol administration. However, the use of cFLI alone fails to reveal the phenotypical identity of cells. In the present study we used double-labeling procedures to identify the neurochemical phenotype of neurons that showed ethanol-induced cFLI in the rat brainstem. METHODS: Individual groups of rats received intraperitoneal injection of ethanol (1.5 g/kg or 3.5 g/kg) or isotonic saline (23 ml/kg). To assess the specificity of cFLI induced by ethanol, we injected other rats with the drug lithium chloride (LiCl; 76 mg/kg). Two hours after injection, rats were killed and their brains were processed for immunohistochemistry. RESULTS: Both doses of ethanol promoted cFLI in several brainstem regions, including the nucleus of the solitary tract (NTS), the locus coeruleus (LC), and the ventrolateral medulla (VLM). Although LiCl caused significant cFLI in the NTS, this drug promoted only minimal cFLI in the VLM and no significant activation in the LC. We found that a significant proportion of tyrosine hydroxylase (TH)-positive neurons coexpressed ethanol-induced cFLI in the VLM (approximately 75-85%), the NTS (approximately 65-75%), and the LC (approximately 30-65%). Additionally, a significant proportion of neuropeptide Y (NPY)-producing neurons in the VLM coexpressed ethanol-induced cFLI (approximately 60-75%). On the other hand, LiCl promoted activation of TH-positive neurons in the VLM and the NTS but failed to stimulate cFLI in TH-producing neurons in the LC or in NPY-producing neurons of the VLM. CONCLUSIONS: Neurons in the rat brainstem that show ethanol-induced c-Fos expression produce catecholamines and NPY. This research demonstrates the usefulness of double-labeling immunohistochemistry procedures for identifying the neurochemical identity of neurons that are activated after ethanol administration.

Animals↗

Evaluation of a fully automated glycoprotein G-2 based assay for the detection of HSV-2 specific IgG antibodies in serum and plasma.

BACKGROUND: Ranking after infections with Chlamydia trachomatis and human papillomavirus, genital herpesvirus is the third most common sexually transmitted disease. The majority of recurrent genital herpes infections are caused by herpes simplex virus type-2 (HSV-2). Seroepidemiological studies on the prevalence of HSV-2 specific IgG antibodies are especially important to study the impact of this infection among risk groups. OBJECTIVE: To evaluate the sensitivity and specificity of the Cobas Core HSV-2 IgG specific assay (available for research use only), that can be run on the Cobas Core fully automated immuno-analyzer. STUDY DESIGN: The Cobas Core HSV-2 specific IgG EIA is based on macro-beads coated with affinity purified glycoprotein G-2 antigen from HSV-2 infected cells. The Cobas Core HSV-2 IgG specific assay was compared with the Chiron rapid immunoblot assay (RIBA), the Gull enzyme-linked immunosorbent assay (EIA) and the Centocor EIA. The respective assays were tested, using 1219 serum samples, from 612 females and 607 males attending the outpatient clinic for sexually transmitted diseases of the Erasmus Medical Center Rotterdam (EMCR). RESULTS: The consensus value, obtained by a concordant result with three out of four assays, demonstrated 350 positive samples (28.7%), 851 negative samples (69.8%) and 18 (1.5%) serum samples with a discordant result. The overall agreement of the Cobas Core HSV-2 EIA against the consensus value was 95.8% and the sensitivity and specificity proved to be 100 and 97.1% respectively. CONCLUSION: The results obtained with the Cobas Core HSV-2 EIA indicate that this is a useful, specific and sensitive assay for the detection of HSV-2 specific IgG antibodies in serum. The advantage of the Cobas Core HVS-2 EIA compared to the other assays, is that this assay can be performed in a fully automated process.

Adolescent↗

Exercise and the regulation of energy intake.

Energy balance is the resultant of ingested calories and energy expenditure and is generally maintained within narrow limits over prolonged periods. Exercise leads to an increase in energy expenditure which is, in the long-term, counteracted by increased energy intake. Evidence for this comes from a study in voluntarily running female rats that increased their daily food intake to 130% of the sedentary controls. In contrast, when considered on a short-term basis, exercise will suppress food intake to prevent a potentially dangerous disruption of energy substrate homeostasis. Studies in permanently cannulated rats submitted to a test meal and 2 hrs swimming reveal that both food intake and exercise lead to increases in glucose and free fatty acid (FFA) levels in the blood. These changes in glucose and FFA, combined with the exercise-induced alteration in among others glucagon, corticotropin releasing hormone (CRH) and body temperature, may lead to the short-term anorexic effect of exercise.

Animals↗

Glucagon-like peptide-1 (7-36) amide: a central regulator of satiety and interoceptive stress.

Glucagon-like peptide-1 (7-36) amide (GLP-1) is processed from proglucagon in the distal ileum as well as in the CNS. In the periphery, GLP-1 acts as an incretin factor and profoundly inhibits upper gastrointestinal motility ('ileal brake'), the latter presumably involving the CNS. Within the CNS, GLP-1 has a satiating effect, since administration of GLP-1 into the third cerebral ventricle reduces short-term food intake (and meal size), while administration of GLP-1 antagonists have the opposite effect. In addition, activation of GLP-1 receptors in certain brain regions elicits strong taste aversions. Similarities between toxin- and GLP-1-induced neuronal activity in the CNS (brain stem) suggest a role for central GLP-1 receptors in relaying interoceptive stress. Thus, regionally distinct GLP-1 receptor populations in the CNS may be involved in satiety or malaise. It is argued that the satiating and aversive aspects of GLP-1 serve homeostatic and nonhomeostatic functions with respect to maintenance of nutrient balance.

Animals↗

Metabolic, gastrointestinal, and CNS neuropeptide effects of brain leptin administration in the rat.

To investigate whether brain leptin involves neuropeptidergic pathways influencing ingestion, metabolism, and gastrointestinal functioning, leptin (3.5 micrograms) was infused daily into the third cerebral ventricular of rats for 3 days. To distinguish between direct leptin effects and those secondary to leptin-induced anorexia, we studied vehicle-infused rats with food available ad libitum and those that were pair-fed to leptin-treated animals. Although body weight was comparably reduced (-8%) and plasma glycerol was comparably increased (142 and 17%, respectively) in leptin-treated and pair-fed animals relative to controls, increases in plasma fatty acids and ketones were only detected (132 and 234%, respectively) in pair-fed rats. Resting energy expenditure (-15%) and gastrointestinal fill (-50%) were reduced by pair-feeding relative to the ad libitum group, but they were not reduced by leptin treatment. Relative to controls, leptin increased hypothalamic mRNA for corticotropin-releasing hormone (CRH; 61%) and for proopiomelanocortin (POMC; 31%) but did not reduce mRNA for neuropeptide Y. These results suggest that CNS leptin prevents metabolic/gastrointestinal responses to caloric restriction by activating hypothalamic CRH- and POMC-containing pathways and raise the possibility that these peripheral responses to CNS leptin administration contribute to leptin's anorexigenic action.

Animals↗

Central infusion of glucagon-like peptide-1-(7-36) amide (GLP-1) receptor antagonist attenuates lithium chloride-induced c-Fos induction in rat brainstem.

Central infusion of glucagon-like peptide-1-(7-36) amide (GLP-1) and intraperitoneal (i.p.) injection of lithium chloride (LiCl) produce similar patterns of c-Fos induction in the rat brain. These similarities led us to assess the hypothesis that neuronal activity caused by i.p. injection of LiCl involves activation of central GLP-1 pathways. We therefore determined if third-ventricular (i3vt) infusion of a GLP-1 receptor antagonist would block LiCl-induced c-Fos expression in the brainstem. Relative to rats pretreated with i3vt infusion of vehicle, pretreatment with the potent GLP-1 receptor antagonist, des His1 Glu9 exendin-4 (10.0 microgram), significantly attenuated LiCl-induced (76 mg/kg; i.p.) c-Fos expression in several brainstem regions, including the area postrema, the nucleus of the solitary tract, and the lateral parabrachial nucleus. While central infusion of des His1 Glu9 exendin-4 also blocked GLP-1-induced (10.0 microgram) anorexia and c-Fos expression, the antagonist produced no independent effects on food intake or c-Fos expression. These results suggest that LiCl-induced c-Fos expression in the rat brainstem is mediated, at least in part, by GLP-1 receptor signaling.

Animals↗

[Efficiency of mixed RASTs in serological screening of possibly allergic patients].

OBJECTIVE: To determine the age distribution of results of serological allergy screening using mixed-allergen radioallergoabsorbent tests (RASTs), and to determine the cost-effectiveness of mix RASTs. DESIGN: Retrospective. SETTING: University Hospital of Rotterdam; Dijkzigt Hospital and Sophia Children's Hospital, the Netherlands. METHODS: An analysis was made of the results of all determinations requested in a period of 3 years with use of the CAP Phadiatop test (aimed at IgE against a mixture of inhalant allergens) and the CAP f x 5 food mix test (aimed at IgE against a mixture of food allergens). RESULTS: The CAP Phadiatop test was positive most strongly and most frequently in patients aged 7 to 30 years. From the age of 2 years, there was a sharp rise of the number of positive CAP Phadiatop tests, but IgE against inhalant allergens was also found in over 10% of the children aged 0 and 1 year. Up to and including the age category of 6 years, over one-third of the sera submitted had a positive CAP f x 5 food mix test. From a budget point of view, preliminary screening with a mix RAST is the more advantageous the lower the allergy prevalence and the higher the mean number of CAP-RASTs to be requested per serum. CONCLUSION: A substantial saving of laboratory costs can be achieved by having mix RASTs such as CAP Phadiatop and CAP f x 5 food mix tests precede determinations of specific IgE against separate allergens; these savings will be the higher the smaller the proportion of positive results and the higher the mean number of separate RASTs to be requested per serum.

Adolescent↗

Intraventricular GLP-1 reduces short- but not long-term food intake or body weight in lean and obese rats.

Glucagon-like-peptide-1 (7-36) amide (GLP-1), when infused into the third ventricle (I.V.T.), reduces short-term food intake. In the present experiments, we assessed whether I.V.T. administration of GLP-1 could influence long-term food intake and body weight of lean Long Evans rats and of fatty Zucker (fa/fa) rats. In Experiment 1, we replicated the observation that 10 microg GLP-1, given I.V.T., reduces one and 2 h food intake, and extended the observation to fatty Zucker rats. However, in both rat strains, 24 h food intake and body weight were unchanged by this acute treatment. In Experiment 2, GLP-1 (30 microg/day) was infused I.V.T. continuously for 4 days via an osmotic mini-pump. This treatment also had no effect on food intake or body weight in either Long-Evans or fatty Zucker rats. A control experiment verified that the GLP-1 remained biologically active over the duration of the infusion period. In a final experiment, Long-Evans rats were restricted to two 2 h periods of access to food each day for 6 days. Prior to each of these access periods, rats received either 15 microg of GLP-1 I.V.T. or a vehicle control injection. While GLP-1 significantly reduced food intake on the first day of treatment, this effect of GLP-1 rapidly disappeared such that it was reduced on the second day and absent on the third day; and there was no effect on body weight at any time. Collectively, the present experiments do not support the hypothesis that GLP-1, acting in the CNS, is an important regulator of long-term food intake and body weight.

Analysis of Variance↗