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Biomedical subjects

H Pijl

Publications and source records attributed to H Pijl.

At least 19 recordsLinked to original sources
PubMed1998

[Overweight. III. Therapeutic strategies for weight reduction].

Obesity is a major health hazard. It increases the risk of cardiovascular disease, diabetes, mellitus and various malignancies. Minor weight loss (5-10% of body weight) appears to reduce this risk. (Very) low calorie diets alone are not effective in the long run. Regular physical exercise and behavioral interventions improve the effect of calorie restriction to an extent that is beneficial to health. Long term drug treatment is not recommended for the treatment of obesity. A number of appetite suppressants has been withdrawn from the market because of serious side effects during long term (> 3 months) use. Also, data on the efficacy of long term (> 1 year) drug treatment of obesity are not available. However, short term use to support calorie restriction might be helpful. Bariatric surgery is indicated and reasonably safe for morbidly obese patients (body mass index > or = 40 kg/m2), particularly for those who have other risk factors for cardiovascular disease. Adjustable gastric banding appears to be an effective and safe alternative to (vertical) gastroplasty.

Anti-Obesity Agents↗
PubMed1998

No effect of consumption of green and black tea on plasma lipid and antioxidant levels and on LDL oxidation in smokers.

Intake of flavonoids is associated with a reduced cardiovascular risk. Oxidation of LDL is a major step in atherogenesis, and antioxidants may protect LDL from oxidation. Because tea is an important source of flavonoids, which are strong antioxidants, we have assessed in a randomized, placebo-controlled study the effect of consumption of black and green tea and of intake of isolated green tea polyphenols on LDL oxidation ex vivo and on plasma levels of antioxidants and lipids. Healthy male and female smokers (aged 34+/-12 years, 13 to 16 per group) consumed during a 4-week period 6 cups (900 mL) of black or green tea or water per day, or they received as a supplement 3.6 grams of green tea polyphenols per day (equivalent to the consumption of 18 cups of green tea per day). Consumption of black or green tea had no effect on plasma cholesterol and triglycerides, HDL and LDL cholesterol, plasma vitamins C and E, beta-carotene, and uric acid. No differences were found in parameters of LDL oxidation. Intake of green tea polyphenols decreased plasma vitamin E significantly in that group compared with the control group (-11% P=.016) but had no effect on LDL oxidation ex vivo. We conclude that consumption of black or green tea (6 cups per day) has no effect on plasma lipids and no sparing effect on plasma antioxidant vitamins and that intake of a high dose of isolated green tea polyphenols decreases plasma vitamin E. Although tea polyphenols had a potent antioxidant activity on LDL oxidation in vitro, no effect was found on LDL oxidation ex vivo after consumption of green or black tea or intake of a green tea polyphenol isolate.

Adult↗
PubMed1998

Circadian rhythm of plasma leptin levels in upper and lower body obese women: influence of body fat distribution and weight loss.

Plasma leptin concentrations were measured every 20 min for 24 h in eight normal weight women and in eight upper body and eight lower body obese women matched for body mass index. The circadian rhythm of leptin, which could mathematically be described by a cosine, was characterized by an acrophase just after midnight in all subjects. The amplitude of a cosine fit as well as the average 24-h leptin concentration were increased by 280% and 420%, respectively, in obese compared to normal weight women. All characteristics of leptin concentration profiles were similar in upper body and lower body obese women, except for a significantly higher amplitude in the lower body obese group. Visceral and sc body fat depots were measured using magnetic resonance imaging in all three groups. Average 24-h leptin concentrations were strongly correlated with sc fat (r = 0.84), whereas visceral fat was not an independent predictor of the plasma leptin level. A loss of 50% of the overweight was associated with a 55% decrease in the average 24-h leptin concentrations in obese women (95% confidence interval, 12.3, 26.6), whereas the characteristics of the circadian rhythm of leptin remained unchanged. Finally, it was observed that a fasting plasma leptin concentration is not an acceptable indicator of the average leptin concentration over 24 h.

Adipose Tissue↗
PubMed1997

Insulin and leptin concentrations in obese humans during long-term weight loss.

BACKGROUND: Leptin is likely to be involved in the homeostasis of body weight. Insulin is suggested to regulate both short-term and long-term circulating leptin levels. The present study aims to assess the relation between insulin and leptin levels in obese humans. METHODS: Some 53 obese subjects (body mass index 35.1 +/- 3.9 kg m-2 (mean +/- SD)) were prescribed a hypocaloric diet and randomized to either a placebo or the intestinal lipase inhibitor orlistat for 2 years. Serum leptin and insulin levels were determined repeatedly during these 2 years (5 times in the fasting condition and twice after an oral glucose load). RESULTS: Leptin concentrations appeared to be regulated at a specific level for each individual throughout the weight-loss period. The BMI explained 39.7% of the total variance in leptin levels, the body-fat distribution 17.2%, individual characteristics 30.3%; and the fasting serum insulin concentration 1.0%. After a mean weight loss of 7.7 +/- 4.9 kg, the time-integrated insulin response to an oral glucose load was significantly lower but the leptin response remained unchanged. CONCLUSIONS: The BMI is the main determinant of the circulating leptin concentration in obese humans. Individual characteristics seem to determine the leptin level, given the BMI. In a short-term observational study in obese humans, changes of insulin levels do not appear to be correlated to changes in leptin levels.

Adult↗
PubMed1997

Psychological and metabolic responses of carbohydrate craving obese patients to carbohydrate, fat and protein-rich meals.

RATIONALE: A defective central serotonergic neurotransmission has been suggested to result in the concomitant occurrence of an appetite disorder and a disturbed mood. This syndrome was termed carbohydrate carving (CC) obesity. Excessive consumption of carbohydrate-rich snacks would, through a plasma amino acid mediated mechanism, restore serotonergic neurotransmission and thereby relieve the symptoms of atypical depression. OBJECTIVES: To test whether CC obese patients indeed exhibit symptoms of atypical depression, whether these symptoms can be alleviated by carbohydrate-rich snacks and whether they respond differently to the snacks than non-carbohydrate craving (NC) control subjects. Furthermore, we investigated whether differences between CC and NC patients could be related to peripheral metabolic differences. DESIGN: Double blinded, randomized with cross-over. Patients received three types of snacks (100/0/0, 70/29/1 and 35/3/62 energy percent carbohydrate/fat/protein respectively) on three consecutive test days. Before and after snack administration mood and performance were tested and blood samples were obtained. SUBJECTS: 9 CC and 17 NC obese patients, matched for sex, age and body mass index. MEASUREMENTS: Mood states (Profile of Mood States and Visual Analogue Scales) and performance (Bourdon-Wiersma cancellation test), serum glucose and insulin and plasma amino acid concentrations. RESULTS: Before snack consumption, CC patients had slightly higher anger and fatigue scores and tended to have lower mood scores than NC patients. The efficiency of performance increased in both groups after all snacks. No other psychological effects of the snacks were registered. Psychological and metabolic responses of CC and NC patients to the snacks were similar. CONCLUSION: Although they may have a somewhat disturbed mood, CC obese patients do not improve their mood states through ingestion of a carbohydrate-rich snack. It seems, from a therapeutic point of view, useless to maintain the concept of carbohydrate craving.

Adult↗
PubMed1997

Predictors of weight loss during treatment with d-fenfluramine.

OBJECTIVE: To identify parameters predictive of weight loss during treatment with d-fenfluramine. This may provide a tool to recognize patients who are sensitive to the weight-reducing effect of d-fenfluramine and thus prevent unnecessary prescription. DESIGN: An open intervention study during which biweekly control visits were scheduled. The study lasted 12 weeks. SETTING: The General Internal Medicine outpatient clinic of the Leiden University Hospital. Patients were recruited through a newspaper advertisement. SUBJECTS: Forty-eight healthy, obese patients (36 women and 12 men), aged 39 +/- 10 years (mean +/- SD) with a body mass index of 34.3 +/- 4.1 kg/m2 enrolled. INTERVENTIONS: d-Fenfluramine 15 mg twice daily for 12 weeks. MAIN OUTCOME MEASURES: Body weight, height, waist and hip circumference, food intake, smoking habits, obesity history, treatment history, family history of obesity and compliance with the medication scheme were recorded as potential predictors of weight loss. RESULTS: One patient was withdrawn because of depressive symptoms. Thirteen patients did not lose weight. On average, the other 34 patients lost 5.7 +/- 2.9 kg or 18.1 +/- 9.4% of excess body weight. High compliance with the drug regimen was associated with a twofold greater weight loss (17.7 +/- 12.3 vs. 9.0 +/- 9.4% of excess weight, ANOVA, P = 0.0088). Patients with a positive family history of obesity lost twice as much weight as patients without obese relatives (15.8 +/- 11.8 vs. 6.0 +/- 7.3% of excess weight; ANOVA, P = 0.0078). No other potential determinants were predictive for weight loss. CONCLUSIONS: Informing patients that compliance with the medication scheme improves treatment outcome will be useful. Previous failures to lose weight should not exclude patients from treatment. A positive family history of obesity needs further evaluation as a possible determinant of weight loss in forthcoming studies.

Adult↗
PubMed1996

Borderline personality, impulsiveness, and platelet monoamine measures in bulimia nervosa and recurrent suicidal behavior.

This study examined the relationship between borderline and impulsive personality traits on the one hand, and monoamine function on the other in 15 women with bulimia nervosa and 15 women with recurrent suicidal behavior. Platelet serotonin (5-HT) and platelet monoamine oxidase (MAO) activity were used as peripheral measures of monoaminergic function. All suicide attempters were diagnosed as having a borderline personality disorder, whereas this diagnosis was less frequent in bulimics. Bulimics with borderline comorbidity resembled recurrent suicide attempters with borderline personality disorder more closely in both psychological (anger, impulsive behavior) and biochemical characteristics (platelet 5-HT) than bulimics without borderline personality disorder. Platelet 5-HT was higher in patients with borderline personality than in normal female controls and was positively correlated with the disposition to experience anger. Impulsive personality traits were consistently negatively correlated with platelet MAO activity. Our findings support the subdivision of bulimics according to the presence of borderline or "multi-impulsive" personality disorder.

Blood Platelets↗
PubMed1996

Leptin.

A highly conserved protein called 'leptin' was recently discovered to play a role in regulation of the energy balance in humans and rodents. This 167-amino-acid-containing protein is only produced and secreted by mature adipocytes. Absence of the protein in mutant ob/ob mice and resistance to its effects in db/db mice lead to extreme obesity and type II diabetes mellitus. No mutation of the ob-gene encoding for leptin has been found in obese humans so far. ob mRNA in adipocytes and serum leptin levels are positively related to adipose tissue mass. Receptors for leptin have been found in the choroid plexus and hypothalamus. A feedback inhibition of leptin on hypothalamic neuropeptide Y (NY) production is postulated, as hypothalamic NY concentrations are increased in ob/ob mice and NY induces food intake, insulin secretion and autonomic nervous system activity. Insulin increases triglyceride stores in fat cells and could thereby stimulate leptin secretion. The ultimate intracellular pathway within the adipocyte that stimulates or shuts off ob mRNA expression and consequent leptin production and secretion remains to be elucidated. Whether leptin will ever come to play a role in the treatment of human obesity remains an unanswered question at the present time.

Adipocytes↗
PubMed1996

Specific stimulation of brain serotonin mediated neurotransmission by dexfenfluramine does not restore growth hormone responsiveness in obese women.

OBJECTIVE: Growth hormone release in response to all known stimuli of GH secretion is blunted in obese subjects. Several studies, using d,l-fenfluramine (d,l-FF) as a serotoninergic tool, suggest that brain serotonin plays a role in the pathogenesis of this phenomenon. However, the effect of d,l-FF appears to be dependent on the stimulus used to induce GH release. Furthermore, d,l-FF has catecholamingergic properties apart from its capacity to stimulate serotonin release and to block its re-uptake. In this study, we investigated whether subchronic treatment with the highly selective serotoninergic drug dexfenfluramine (d-FF) affects the GH response to galanin or GHRH in obese subjects. DESIGN: The study had a randomized, cross-over, placebo controlled design. d-FF was administered in a dose of 15 mg twice daily during 6 days. On days 5 and 6 of treatment (with either d-FF or placebo) an i.v. bolus injection of 100 micrograms hGHRH(1-44) or a continuous infusion of p-galanin (40 pmol/kg/min over 40 minutes) were administered in randomized order. All tests were performed in the follicular phase of two consecutive menstrual cycles. PATIENTS: Eight obese women (body mass index (BMI) 34.5 +/- 3.6 kg/m2); 7 normal weight (BMI 21.9 +/- 1.9 kg/m2) age-matched control women. All women had a regular menstrual cycle. None used oral contraceptive drugs. MEASUREMENTS: GH response to either stimulus was measured both during treatment with d-FF and during treatment with placebo. RESULTS: The GH response to galanin and the response to GHRH were significantly smaller in obese subjects. d-FF significantly reduced the galanin induced GH secretion in obese subjects, but not in normal weight controls. It did not significantly affect GH release in response to GHRH in either group. CONCLUSION: This study confirms that GH secretion in response to stimuli with varying mechanisms of action is blunted in obese subjects. A decrease of central serotonin mediated neurotransmission does not appear to play a role in the pathogenesis of this phenomenon.

Adult↗
PubMed1996

Bodyweight change as an adverse effect of drug treatment. Mechanisms and management.

A number of drugs are capable of changing bodyweight as an adverse effect of their therapeutic action. Bodyweight gain is more of a problem than bodyweight loss. As bodyweight gain during drug treatment for any kind of disease may be the reflection of improvement of the disease itself, we will try to separate these effects from those due to drug-induced alterations of the mechanisms regulating bodyweight. Bodyweight gain may jeopardise patient compliance to the prescribed regimen and it may pose health risks. The body mass index (BMI) is determined by dividing bodyweight in kilograms by height in metres squared. A BMI of > or = 27 kg/m2 warrants therapeutic action; nutritional counselling and programmed physical exercise can be used as a basis. In general, if basic therapeutic measures are unsuccessful at controlling bodyweight gain then a change of drug might help. Finally, an anoretic drug may serve to support dietary measures. However, safety and efficacy has been demonstrated for only a few anorectic drugs when used as an adjunct to caloric restriction in the treatment of drug-induced obesity. Bodyweight is determined by complex mechanisms regulating energy balance. A number of neurotransmitter systems acting in several hypothalamic nuclei are pivotal to the regulation of body fat stores. Most drugs that are capable of changing bodyweight interfere with these neurotransmitter systems. The increment is dependent on the type and dose of the drug concerned. Some antidepressant drugs induce bodyweight gain, which may amount to 20 kg over several months of treatment. Monoamine oxidase inhibitors appear to cause less bodyweight change than tricyclic antidepressants. Selective serotonin (5-hydroxytryptamine; 5-HT) reuptake inhibitors cause bodyweight loss instead of bodyweight gain. Lithium may cause large increases in bodyweight. Generally speaking, the bodyweight change induced by antipsychotics is more often of clinical significance than the bodyweight change associated with the use of antidepressants. Again, the changes of bodyweight are dependent upon the type and dose of the antipsychotic drug involved. Although almost all antipsychotics induce bodyweight gain, molindone and loxapine appear to induce bodyweight loss. Anticonvulsants, especially valproic acid (sodium valproate) and carbamazepine, induce bodyweight gain in a considerable percentage of patients. Treatment with corticosteroids is associated with dose-dependent bodyweight gain in many patients. Corticosteroid-induced obesity aggravates other corticosteroid-associated health risks. Insulin therapy in diabetic patients usually increases bodyweight. Finally, sulphonurea derivatives, antineoplastic agents used for the treatment of breast cancer and several drugs used in migraine prophylaxis may cause bodyweight gain as well.

Antineoplastic Agents↗
PubMed1996

Serotoninergic drug-induced weight loss in carbohydrate craving obese patients.

RATIONALE: Serotoninergic neurotransmission, mainly in specific hypothalamic nuclei, plays an important role in the regulation of appetite. Dysfunction of this system has been postulated to result in the clinical picture of carbohydrate craving obesity. This subgroup of obese patients is characterized by a specific preference for high-carbohydrate and low-protein snacks. Centrally acting serotoninergic drugs, such as the serotonin re-uptake inhibitor d-fenfluramine, have been hypothesized to restore serotonin mediated control of food intake. OBJECTIVE: To test the hypothesis that serotoninergic drugs would induce a greater weight loss in carbohydrate craving (CC) than in non-carbohydrate craving (NC) obese patients. DESIGN: A three months open intervention study with d-fenfluramine 15 mg twice daily. In order to be able to study the effect of the drug alone, no dietary restrictions were imposed. Both the medical doctor and the patient were unaware of who was a carbohydrate craving obese patient and who was not. SUBJECTS: 10 CC and 10 NC patients, matched for sex, age, body mass index and family history of obesity. MEASUREMENTS: Height, body weight, food intake (energy intake and macronutrient selection) and patient compliance. RESULTS: CC patients lost 4.8 +/- 3.9 kg body weight or 15.9 +/- 13.5% of their pretreatment overweight, whereas NC patients lost 4.5 +/- 2.9 kg or 16.4 +/- 11.6% of their overweight (t-test for paired samples, P = 0.82 and P = 0.93 respectively). CONCLUSION: We conclude that CC patients do not constitute a subgroup of obese patients that should be treated with a serotoninergic drug preferentially.

Appetite Depressants↗
PubMed1995

Plasma amino acid ratios related to brain serotonin synthesis in response to food intake in bulimia nervosa.

Fifteen bulimic women (BN) and 19 healthy female controls (CO) were studied. The subjects were cross-over treated with either fluoxetine (FXT) or placebo during 4 days. They received, in randomized order, a breakfast containing pure carbohydrate (CHO) or a protein-rich (PROT) breakfast following day 3 and 4 of each treatment period. Twenty-nine different food items were offered for lunch. The fasting serum glucose and insulin concentrations and the fasting plasma tryptophan (Trp)/large neutral amino acid (LNAA) ratio were slightly higher in BN. The changes of these metabolic parameters in response to a CHO or PROT breakfast were similar in both groups. Across breakfast type, the plasma (Trp)/(LNAA) ratio at 120 min after breakfast was higher in BN. Total caloric intake at lunchtime was less in BN. In CO, less carbohydrate was selected at lunchtime following the CHO breakfast, an effect that was abolished by FXT. Breakfast type or FXT did not have any apparent effect on food intake at lunchtime in BN. This might indicate that bulimic subjects are less sensitive to serotoninergic stimuli than control subjects.

Adult↗
PubMed1995

Stress, serotonergic function, and mood in users of oral contraceptives.

The relationship between stress and changes in insulin levels, plasma ratio of tryptophan to other large neutral amino acids (LNAAs), mood, and food intake was investigated in women taking monophasic oral contraceptives containing progestagens. Subjects experiencing high levels of stress displayed significant decreases of insulin and tryptophan to other LNAAs ratios, before and after the consumption of a standard meal during the pill-free period as compared with the period of pill use. The decline of the tryptophan to other LNAAs ratio was accompanied by worsening of mood. In a control group of subjects experiencing low levels of stress there was no relationship between insulin and tryptophan to other LNAAs ratio, nor between tryptophan to other LNAAs ratio and mood. These results suggest that the combination of stress and alterations in sex hormones may be responsible for mood changes during the pill-free period in women taking oral contraceptives.

Adult↗