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Biomedical subjects

W H M Saris

Publications and source records attributed to W H M Saris.

At least 19 recordsLinked to original sources
PubMed2006

Substrate source utilisation in long-term diagnosed type 2 diabetes patients at rest, and during exercise and subsequent recovery.

AIMS/HYPOTHESIS: Disturbances in substrate source metabolism and, more particularly, in fatty acid metabolism, play an important role in the aetiology and progression of type 2 diabetes. However, data on substrate source utilisation in type 2 diabetes are inconclusive. METHODS: [U-(13)C]palmitate and [6,6-(2)H(2)]glucose tracers were used to assess plasma NEFA and glucose oxidation rates and to estimate the use of muscle- and/or lipoprotein-derived triacylglycerol and muscle glycogen. Subjects were ten male patients who had a long-term (7 +/- 1 years) diagnosis of type 2 diabetes and were overweight, and ten matched healthy, male control subjects. Muscle biopsy samples were collected before and after exercise to assess muscle fibre type-specific intramyocellular lipid and glycogen content. RESULTS: At rest and during exercise, the diabetes patients had greater values than the controls for palmitate rate of appearance (Ra) (rest, 2.46 +/- 0.18 and 1.85 +/- 0.20 respectively; exercise, 3.71 +/- 0.36 and 2.84 +/- 0.20 micromol kg(-1) min(-1)) and rate of disappearance (Rd) (rest, 2.45 +/- 0.18 and 1.83 +/- 0.20; exercise, 3.64 +/- 0.35 and 2.80 +/- 0.20 micromol kg(-1) min(-1) respectively). This was accompanied by significantly higher fat oxidation rates at rest and during recovery in the diabetes patients (rest, 0.11 +/- 0.01 in diabetes patients and 0.09 +/- 0.01 in controls; recovery, 0.13 +/- 0.01 and 0.11 +/- 0.01 g/min respectively), despite significantly greater plasma glucose Ra, Rd and circulating plasma glucose concentrations. Furthermore, exercise significantly lowered plasma glucose concentrations in the diabetes patients, as a result of increased blood glucose disposal. CONCLUSION: This study demonstrates that substrate source utilisation in long-term-diagnosed type 2 diabetes patients, in whom compensatory hyperinsulinaemia is no longer present, shifts towards an increase in whole-body fat oxidation rate and is accompanied by disturbances in fat and carbohydrate handling.

Biopsy↗
PubMed2006

Association of a beta-2 adrenoceptor (ADRB2) gene variant with a blunted in vivo lipolysis and fat oxidation.

BACKGROUND AND AIMS: Obesity is associated with a blunted beta-adrenoceptor-mediated lipolysis and fat oxidation. We investigated whether polymorphisms in codon 16, 27 and 164 of the beta (2)-adrenoceptor gene (ADRB2) and exon 10 of the G protein beta (3)-subunit gene (GNB3) are associated with alterations in in vivo lipolysis and fat oxidation. DESIGN AND METHODS: Sixty-five male and 43 female overweight and obese subjects (body mass index (BMI) range: 26.1-48.4 kg/m(2)) were included. Energy expenditure (EE), respiratory quotient (RQ), circulating free fatty acid (FFA) and glycerol levels were determined after stepwise infusion of increasing doses of the non-selective beta-agonist isoprenaline (ISO). RESULTS: In women, the Arg16 allele of the ADRB2 gene was associated with a blunted increase in circulating FFA, glycerol and a decreased fat oxidation during ISO stimulation. In men, the Arg16 allele was significantly associated with a blunted increase in FFA but not in glycerol or fat oxidation. CONCLUSION: These results suggest that genetic variation in the ADRB2 gene is associated with disturbances in in vivo beta-adrenoceptor-mediated lipolysis and fat oxidation during beta-adrenergic stimulation in overweight and obese subjects; these effects are influenced by gene-gender interactions.

Adipose Tissue↗
PubMed2006

Effect of short-term ACE inhibitor treatment on peripheral insulin sensitivity in obese insulin-resistant subjects.

AIMS/HYPOTHESIS: This study was designed to investigate the effect of short-term ACE inhibitor treatment on insulin sensitivity and to examine possible underlying metabolic and haemodynamic effects in obese insulin-resistant subjects. METHODS: A randomised, double-blind placebo-controlled trial was performed in 18 obese insulin-resistant men (age, 53 +/- 2 years; BMI, 32.6 +/- 0.8 kg/m(2); homeostasis model assessment of insulin resistance, 5.6 +/- 0.5; systolic blood pressure [SBP], 140.8 +/- 3.2; diastolic blood pressure [DBP], 88.8 +/- 1.6 mmHg), who were free of any medication. The aim was to examine the effects of 2 weeks of ACE inhibitor treatment (ramipril, 5 mg/day) on insulin sensitivity, forearm blood flow, substrate fluxes across the forearm, whole-body substrate oxidation and intramuscular triacylglycerol (IMTG) content. RESULTS: Ramipril treatment decreased ACE activity compared with placebo (-22.0 +/- 1.7 vs 0.2 +/- 1.1 U/l, respectively, p < 0.001), resulting in a significantly reduced blood pressure (SBP, -10.8 +/- 2.1 vs -2.7 +/- 2.0 mmHg, respectively, p = 0.01; DBP, -10.1 +/- 1.3 vs -4.2 +/- 2.1 mmHg, respectively, p = 0.03). Ramipril treatment had no effect on whole-body insulin-mediated glucose disposal (before: 17.9 +/- 2.0, after: 19.1 +/- 2.4 micromol kg body weight(-1) min(-1), p = 0.44), insulin-mediated glucose uptake across the forearm (before: 1.82 +/- 0.39, after: 1.92 +/- 0.29 micromol 100 ml forearm tissue(-1) min(-1), p = 0.81) and IMTG content (before: 45.4 +/- 18.8, after: 48.8 +/- 27.5 micromol/mg dry muscle, p = 0.92). Furthermore, the increase in carbohydrate oxidation (p < 0.001) and forearm blood flow (p < 0.01), and the decrease in fat oxidation (p < 0.001) during insulin stimulation were not significantly different between treatments. CONCLUSIONS/INTERPRETATION: Short-term ramipril treatment adequately reduced ACE activity and blood pressure, but had no significant effects on insulin sensitivity, forearm blood flow, substrate fluxes across the forearm, whole-body substrate oxidation and IMTG content in obese insulin-resistant subjects.

Angiotensin II↗
PubMed2006

Improvements in glucose tolerance and insulin sensitivity after lifestyle intervention are related to changes in serum fatty acid profile and desaturase activities: the SLIM study.

AIMS/HYPOTHESIS: The aim of this study was to investigate whether lifestyle intervention-induced changes in serum fatty acid profile of cholesteryl esters and estimated desaturase activities are related to improvements in insulin sensitivity in subjects at risk of type 2 diabetes. MATERIALS AND METHODS: In the Study on Lifestyle Intervention and Impaired Glucose Tolerance Maastricht (SLIM), 97 men and women with IGT were randomised to a combined diet and exercise programme (47 intervention) or a control group (50 control subjects). At baseline and after 1 year the following assessments were made: an OGTT, an exercise test to determine maximal aerobic capacity, anthropometry, and analysis of the serum fatty acid profile of cholesteryl esters. RESULTS: The lifestyle programme was effective in reducing the intake of total and saturated fat, increasing physical activity, reducing obesity and improving insulin sensitivity and glucose tolerance. Regression analysis of the total population showed that an increase in the C20:4 n-6/C20:3 n-6 ratio (estimated Delta5-desaturase activity) and reductions in the C18:3 n-6/C18:2 n-6 ratio (estimated Delta6-desaturase activity) and the C16:1 n-7/C16:0 ratio (estimated Delta9-desaturase activity or stearoyl-CoA desaturase-1) were significantly associated with a decrease in homeostasis model assessment for insulin resistance. After adjustment for lifestyle changes (change in percentage body fat, aerobic capacity and saturated fat intake), these associations were partly reduced, but remained statistically significant. CONCLUSIONS/INTERPRETATION: Lifestyle-induced changes in fatty acid profile of cholesteryl esters and desaturase activities were independently related to changes in insulin sensitivity in subjects at risk of type 2 diabetes.

Blood Glucose↗
PubMed2006

Peroxisome proliferator-activated receptor-gamma coactivator-1 and insulin resistance: acute effect of fatty acids.

AIMS/HYPOTHESIS: Peroxisome proliferator-activated receptor (PPAR)-gamma coactivator-1 (PPARGC1), a coactivator regulating the transcription of genes involved in oxidative metabolism, is downregulated in patients with type 2 diabetes and in their first-degree relatives. Whether this downregulation is a cause or effect of early aberrations in the development of insulin resistance, such as disturbances in fat metabolism, is unknown. We examined whether lipid-induced insulin resistance was associated with downregulation of expression of skeletal muscle genes involved in oxidative metabolism and mitochondrial biogenesis in humans. MATERIALS AND METHODS: Nine healthy lean male subjects underwent a 6-h hyperinsulinaemic-euglycaemic clamp with simultaneous infusion of either a lipid emulsion or glycerol as a control. Blood was sampled at regular time points and muscle biopsies were taken before and after every test. Intramuscular triacylglycerol (IMTG) content was determined by Oil Red O staining and gene expression was measured by quantitative PCR. RESULTS: Lipid infusion resulted in a approximately 2.7-fold increase in plasma NEFA levels and a 31+/-6% decrease in insulin sensitivity (p=0.001). The infusion of lipids resulted in a approximately 1.6-fold increase in IMTG (p=0.02), whereas during the clamp with glycerol infusion IMTG tended to decrease to approximately 53% of preinfusion levels (p=0.065). Lipid infusion decreased PPARGC1A, PPARGC1B and PPARA expression to approximately 61, 77 and approximately 52% of basal values respectively, whereas expression of uncoupling protein 3 was upregulated 1.8-fold (all p<0.05). CONCLUSIONS/INTERPRETATION: Acute elevation of plasma NEFA levels, leading to muscular fat accumulation and insulin resistance, downregulates PPARGC1A, PPARGC1B and PPARA expression, suggesting that the decrease in PPARGC1 expression observed in the (pre)diabetic state may be the result, rather than the cause of lipid-induced insulin resistance.

Adult↗
PubMed2006

Angiotensin II: a hormone that affects lipid metabolism in adipose tissue.

BACKGROUND: Alterations in adipose tissue lipolysis may contribute to the pathophysiology of obesity and insulin resistance. We examined the effects of angiotensin II (Ang II) on abdominal subcutaneous adipose tissue lipolysis in humans. METHODS AND RESULTS: First, adipocytes obtained from nine normal weight and seven obese subjects were stimulated with Ang II (10(-14)-10(-6) M). Glycerol concentration in the medium, used as an indicator of adipocyte lipolysis, was significantly reduced (approximately 20%) after Ang II stimulation in adipocytes from normal weight (P=0.04) and obese subjects (P<0.001). Based on these observations, adipocytes of seven additional obese subjects were stimulated with lower doses of Ang II (10(-17)-10(-6) M) in the presence and absence of Ang II type 1 (AT(1)) receptor blockade. Lipolysis was dose dependently inhibited by approximately 20 to 25% after Ang II stimulation (P=0.001). AT(1) receptor blockade completely abolished the Ang II-induced effects (P=0.35). CONCLUSION: Ang II directly inhibits abdominal subcutaneous adipocyte lipolysis in normal weight and obese subjects via the AT(1) receptor.

Adipocytes↗
PubMed2006

Short-term training is accompanied by a down regulation of ACC2 mRNA in skeletal muscle.

Recently, we showed that short-term training induced a rapid increase in IMCL whilst insulin sensitivity tended to improve. Here we investigate molecular adaptations accompanying this physiological training-induced accumulation of IMCL. Nine untrained men (age: 23.3 +/- 3.2 y; maximal power output: 3.8 +/- 0.6 W/kg body weight) trained for two weeks. Before and after training, subjects cycled for three hours and biopsies were taken before and after exercise. mRNA concentrations of ACC2, HSL, LPL, Glut4 and HKII were quantified by RT-PCR and association of Glut4 with the membrane was quantified by immunohistochemical method. Endurance training resulted in a decrease of 29.1 % in ACC2 mRNA (p = 0.02). After training, ACC2 mRNA tended to decrease with acute exercise (- 24.4 % [p = 0.06]). HSL mRNA decreased with acute exercise after training (- 37.3 % [p = 0.002]). LPL mRNA concentrations increased with acute exercise before training (+ 42.4 % [p = 0.05]) and HKII mRNA increased with acute exercise before (+ 72.5 % [p = 0.025]) and after training (+ 99.3 % [p = 0.05]). After acute exercise, more Glut4 was associated with the membrane than before exercise, but it was not affected by training. We conclude that the training-induced increase in IMCL was accompanied by molecular adaptations in muscle to improve fat oxidative capacity, while markers of glucose metabolism were not yet changed. The present data are in line with the hypothesis that the fat oxidative capacity might be more important than the IMCL content in determining insulin sensitivity.

Acetyl-CoA Carboxylase↗
PubMed2006

[Insulin resistance: the role of intramuscular triglyceride and the importance of physical activity].

In the Netherlands, the prevalence of diabetes is expected to rise from 480,000 to more than 650,000 patients by the year 2020. Numerous studies have reported a strong correlation between elevated plasma-free fatty-acid levels, the accumulation of intramuscular triglyceride (IMTG) and the development of insulin resistance. Traditionally, the Randle cycle was used to explain the mechanism behind fatty acid-induced insulin resistance in skeletal muscle. An alternative explanation is that the increased supply of free fatty acids leads to the accumulation of IMTG and fatty-acid metabolites, which can induce defects in the insulin signalling cascade, causing insulin resistance in skeletal muscle. However, this proposed relationship between elevated IMTG concentrations and skeletal-muscle insulin resistance does not always apply, as trained athletes have been shown to be markedly insulin-sensitive, despite having high levels of stored IMTG. This metabolic paradox is explained by the fact that it is not the size of the IMTG pool but rather the balance between fatty-acid availability, uptake and oxidation, i.e. the low turnover of the IMTG pool, that is instrumental in the development of skeletal-muscle insulin resistance. Physical exercise forms an effective strategy to improve the balance between skeletal-muscle fatty-acid uptake and oxidation and, as such, can prevent the development of skeletal-muscle insulin resistance.

Diabetes Mellitus, Type 2↗
PubMed2006

Angiotensin II: a major regulator of subcutaneous adipose tissue blood flow in humans.

We investigated the functional roles of circulating and locally produced angiotensin II (Ang II) in fasting and postprandial adipose tissue blood flow (ATBF) regulation and examined the interaction between Ang II and nitric oxide (NO) in ATBF regulation. Local effects of the pharmacological agents (or contralateral saline) on ATBF, measured with 133Xe wash-out, were assessed using the recently developed microinfusion technique. Fasting and postprandial (75 g glucose challenge) ATBF regulation was investigated in nine lean healthy subjects (age, 29 +/- 3 years; BMI, 23.4 +/- 0.7 kg m(-2)) using local Ang II stimulation, Ang II type 1 (AT1) receptor blockade, and angiotensin-converting enzyme (ACE) inhibition. Furthermore, NO synthase (NOS) blockade alone and in combination with AT1 receptor blockade was used to examine the interaction between Ang II and NO. Ang II induced a dose-dependent decrease in ATBF (10(-9)m: -16%, P = 0.04; 10(-7)m: -33%, P < 0.01; 10(-5)m: -53%P < 0.01). Fasting ATBF was not affected by ACE inhibition, but was increased by approximately 55% (P < 0.01) by AT(1) receptor blockade. NOS blockade induced a approximately 30% (P = 0.001) decrease in fasting ATBF. Combined AT1 receptor and NOS blockade increased ATBF by approximately 40% (P = 0.003). ACE inhibition and AT1 receptor blockade did not affect the postprandial increase in ATBF. We therefore conclude that circulating Ang II is a major regulator of fasting ATBF, and a major proportion of the Ang II-induced decrease in ATBF is NO independent. Locally produced Ang II does not appear to regulate ATBF. Ang II appears to have no major effect on the postprandial enhancement of ATBF.

Adipose Tissue↗
PubMed2006

Randomized, multi-center trial of two hypo-energetic diets in obese subjects: high- versus low-fat content.

OBJECTIVE: To investigate whether a hypo-energetic low-fat diet is superior to a hypo-energetic high-fat diet for the treatment of obesity. DESIGN: Open-label, 10-week dietary intervention comparing two hypo-energetic (-600 kcal/day) diets with a fat energy percent of 20-25 or 40-45. SUBJECTS: Obese (BMI >or=30 kg/m(2)) adult subjects (n = 771), from eight European centers. MEASUREMENTS: Body weight loss, dropout rates, proportion of subjects who lost more than 10% of initial body weight, blood lipid profile, insulin and glucose. RESULTS: The dietary fat energy percent was 25% in the low-fat group and 40% in the high-fat group (mean difference: 16 (95% confidence interval (CI) 15-17)%). Average weight loss was 6.9 kg in the low-fat group and 6.6 kg in the high-fat group (mean difference: 0.3 (95% CI -0.2 to 0.8) kg). Dropout was 13.6% (n = 53) in the low-fat group and 18.3% (n = 70) in the high-fat group (P=0.001). Among completers, more subjects lost >10% in the low-fat group than in the high-fat group ((20.8%, n = 70) versus (14.7%, n = 46), P = 0.02). Fasting plasma total, low-density lipoprotein- and high-density lipoprotein-cholesterol decreased in both groups, but more so in the low-fat group than in the high-fat group. Fasting plasma insulin and glucose were lowered equally by both diets. CONCLUSIONS: The low-fat diet produced similar mean weight loss as the high-fat diet, but resulted in more subjects losing >10% of initial body weight and fewer dropouts. Both diets produced favorable changes in fasting blood lipids, insulin and glucose.

Adult↗
PubMed2006

Microarray profiling of human white adipose tissue after exogenous leptin injection.

BACKGROUND: Leptin is a secreted adipocyte hormone that plays a key role in the regulation of body weight homeostasis. The leptin effect on human white adipose tissue (WAT) is still debated. OBJECTIVE: The aim of this study was to assess whether the administration of polyethylene glycol-leptin (PEG-OB) in a single supraphysiological dose has transcriptional effects on genes of WAT and to identify its target genes and functional pathways in WAT. MATERIALS AND METHODS: Blood samples and WAT biopsies were obtained from 10 healthy nonobese men before treatment and 72 h after the PEG-OB injection, leading to an approximate 809-fold increase in circulating leptin. The WAT gene expression profile before and after the PEG-OB injection was compared using pangenomic microarrays. Functional gene annotations based on the gene ontology of the PEG-OB regulated genes were performed using both an 'in house' automated procedure and GenMAPP (Gene Microarray Pathway Profiler), designed for viewing and analyzing gene expression data in the context of biological pathways. RESULTS: Statistical analysis of microarray data revealed that PEG-OB had a major down-regulated effect on WAT gene expression, as we obtained 1,822 and 100 down- and up-regulated genes, respectively. Microarray data were validated using reverse transcription quantitative PCR. Functional gene annotations of PEG-OB regulated genes revealed that the functional class related to immunity and inflammation was among the most mobilized PEG-OB pathway in WAT. These genes are mainly expressed in the cell of the stroma vascular fraction in comparison with adipocytes. CONCLUSION: Our observations support the hypothesis that leptin could act on WAT, particularly on genes related to inflammation and immunity, which may suggest a novel leptin target pathway in human WAT.

Adipocytes↗
PubMed2006

Direct association of a promoter polymorphism in the CD36/FAT fatty acid transporter gene with Type 2 diabetes mellitus and insulin resistance.

AIMS: The membrane-bound fatty acid transporter CD36/FAT may play a role in disturbed fatty acid handling as observed in the metabolic syndrome and Type 2 diabetes mellitus (T2DM). Genetic variation in the CD36 gene may contribute to the aetiology of diabetes. METHODS: A population-based cohort in the Netherlands [age > 40 years and body mass index (BMI) > 25 kg/m2] of 675 subjects was phenotyped with respect to glucose metabolism with an oral glucose tolerance test and was genotyped for a known 478C-->T substitution and a C/T snp in the upstream promoter region (rs1527479) in the CD36 gene. RESULTS: T2DM was more prevalent in the TT genotype than in the CC genotype. This was most pronounced in women and in subjects with a high BMI (BMI > 27 kg/m2). In addition, within the group of diabetic patients, the TT genotype was commoner in subjects with increased homeostasis model assessment (HOMA) index for insulin resistance. The 478C-->T substitution, previously found in the Japanese population, was not found in our caucasian population. CONCLUSIONS: This is the first study to show a direct association of a CD36 snp with T2DM. Moreover, within the diabetic subjects, this CD36 snp was associated with insulin resistance (HOMA index).

Aged↗
PubMed2005

Inhibition of adipose tissue lipolysis increases intramuscular lipid use in type 2 diabetic patients.

AIMS/HYPOTHESIS: In the present study, we investigated the consequences of adipose tissue lipolytic inhibition on skeletal muscle substrate use in type 2 diabetic patients. MATERIALS AND METHODS: We studied ten type 2 diabetic patients under the following conditions: (1) at rest; (2) during 60 min of cycling exercise at 50% of maximal workload capacity and subsequent recovery. Studies were done under normal, fasting conditions (control trial: CON) and following administration of a nicotinic acid analogue (low plasma non-esterified fatty acid trial: LFA). Continuous [U-13C]palmitate and [6,6 -2H2]glucose infusions were applied to quantify plasma NEFA and glucose oxidation rates, and to estimate intramuscular triacylglycerol (IMTG) and glycogen use. Muscle biopsies were collected before and after exercise to determine net changes in lipid and glycogen content specific to muscle fibre type. RESULTS: Following administration of the nicotinic acid analogue (Acipimox), the plasma NEFA rate of appearance was effectively reduced, resulting in lower NEFA concentrations in the LFA trial (p<0.001). Plasma NEFA oxidation rates were substantially reduced at rest, during exercise and subsequent recovery in the LFA trial. The lower plasma NEFA oxidation rates were compensated by an increase in IMTG and endogenous carbohydrate use (p<0.05). Plasma glucose disposal rates did not differ between trials. In accordance with the tracer data, a greater net decline in type I muscle fibre lipid content was observed following exercise in the LFA trial (p<0.05). CONCLUSIONS/INTERPRETATION: This study shows that plasma NEFA availability regulates IMTG use, and that adipose tissue lipolytic inhibition, in combination with exercise, could be an effective means of augmenting intramuscular lipid and glycogen use in type 2 diabetic patients in an overnight fasted state.

Adipose Tissue↗
PubMed2005

The relation between calcium intake and body composition in a Dutch population: The Amsterdam Growth and Health Longitudinal Study.

To investigate whether dietary calcium intake is related to body mass index and the sum of four skinfolds among subjects in the Amsterdam Growth and Health Longitudinal Study (the Netherlands), the authors followed a cohort of men and women from age 13 years in 1977 to age 36 years in 2000. Longitudinal linear regression analyses were performed with generalized estimating equations in continuous and categorical models, with adjustment for possible confounders. Results showed that calcium intake during adolescence is a weak predictor of calcium intake in adulthood. In this population, only a slight indication was found of a weak inverse relation of calcium intake with body composition. No differences were observed between the middle (800-1,200 mg/day) and high (>1,200 mg/day) groups of calcium intake, suggesting a threshold of approximately 800 mg/day above which calcium intake has no additional beneficial effect on body composition.

Adolescent↗
PubMed2005

Assessment of body composition and breast milk volume in lactating mothers in pastoral communities in Pokot, Kenya, using deuterium oxide.

BACKGROUND: In sub-Saharan Africa, the practice of breast-feeding infants is common. Records documenting the intake of breast milk amongst infants are limited. This study evaluated the association between maternal body composition and the intake of breast milk in infants from the pastoral communities within Pokot, Kenya. METHODS: The study was conducted in 10 lactating mothers who were participating in a longitudinal study aimed at determining maternal body composition, iron stores and vitamin A status during the third trimester pregnancy and four months after they had given birth. Maternal and infant anthropometric measurements were made, and maternal blood samples were taken to determine serum retinol and ferritin levels. Infant milk intake and maternal fat-free mass (FFM) and percent body fat (% BF) were measured using 'the dose to the mother method'. A measured deuterium oxide ((2)H(2)O) dose was given to the mother. Urine and breast milk from the mother, and saliva samples from the infant, were collected on days 1, 8 and 14 after dosing. RESULTS: The mean (+/- SD) maternal mid upper arm circumference (MUAC) and body mass index (BMI) were 21.8 (0.9) cm and 18.6 (1.0) kg/height (m(2)), respectively. Infant weight and weight/age Z score were 4.956 (0.874) kg and -1.750 (0.77), respectively. Throughout the study, the infants gained 20 (4) g/day in body weight and had a milk intake of 555 (22) ml/day. The energy intake of the infant was 1,602 (148) kJ/day and was lower (p < 0.05) than the 2,404 (423) kJ/day estimated requirement by the FAO/WHO/UNU. The maternal FFM, %BF, Hb, Hct, ferritin and retinol were 32.8 (3.1) kg, 17.24 (7.0), 11.5 (1.3) g/dl, 33.9 (4.9), 16.2 (0.1) microg/l and 0.894 (0.16) micromol/l, respectively. Infant milk intake was significantly and positively correlated to maternal pregnancy triceps (r = 0.679) p < 0.05) and pregnancy MUAC (r = 0.725) p < 0.05). Maternal pregnancy MUAC was an important predictor of infant breast milk intake. CONCLUSION: Data on volume of breast milk consumed by the infants suggests, at least for this group of infants, that adequate growth may not be achieved. There is a possibility that lactating mothers practicing exclusive breast-feeding and living under harsh conditions may experience periods of low breast milk volume. Body composition and biochemical findings among this group of Pokot mothers indicate dietary inadequacies that require nutritional intervention.

Arm↗
PubMed2005

beta2-adrenergic receptor polymorphisms and salbutamol-stimulated energy expenditure.

The beta-adrenergic system is involved in the control of energy metabolism and expenditure. The beta2-adrenergic receptor (beta2-AR) gene shows polymorphisms that have been associated with obesity in several studies. In vitro and in vivo studies suggest differences in beta2-AR-mediated function between these polymorphisms. The aim of this study was to investigate the influence of genetic variation in codon 16 of the beta2-AR gene on energy metabolism in humans. Thirty-four subjects were recruited [Gly16Gly (n = 13), Gly16Arg (n = 16), or Arg16Arg (n = 5)]. The beta2-AR was stimulated with two doses of salbutamol (50 and 100 ng/kg fat-free mass per minute) after blockade of the beta1-adrenergic receptors with atenolol. Energy expenditure and plasma substrate and hormone concentrations were measured. The increase in energy expenditure (DeltaEE) was significantly different among groups in which the Arg16Arg group showed the lowest increase (P < 0.05 vs. Gly carriers). In a multiple regression model, variations in the increase in nonesterified fatty acid concentration during salbutamol infusion (partial r = 0.51) and the polymorphism contributed significantly to the variation in DeltaEE. Thirty-five percent of the variation in DeltaEE was explained by these two factors. We conclude that subjects with the Arg16Arg polymorphism of the beta2-AR gene have a reduced thermogenic response to beta2-adrenergic stimulation. Although this relatively small study needs confirmation, the findings support a role for this polymorphism in the development and maintenance of overweight and obesity.

Adult↗
PubMed2005

Netherlands research programme weight gain prevention (NHF-NRG): rationale, objectives and strategies.

OBJECTIVE: To outline the rationale, objectives and strategies used in a systematically designed research programmme to study specific weight gain-inducing behaviours, their social-psychological as well as environmental determinants, and the effects of interventions aimed at the prevention of weight gain. DESIGN: The evidence for potential behavioural determinants and strategies to prevent weight gain was reviewed, and the methods applied within the Netherlands Research programme weight gain prevention (NHF-NRG) project were described. The project is designed according to the Intervention Mapping protocol. SETTING: The Netherlands. SUBJECTS: The main target groups are (a) adolescents (12-16 y) in secondary school, (b) young adults (20-40 y) at the workplace and (c) recently retired people (55-65 y) at home. INTERVENTIONS: Each intervention includes an individual component, in which computer-tailored information is provided. Additionally, interventions are aimed at changing environmental components. RESULTS: The short-term results of this project can be expected by the beginning of 2005. Guidelines for nationwide weight gain prevention, based on this research programme, will become available in 2007. CONCLUSIONS: Based on the few interventions that were evaluated to date, no robust conclusions can be drawn regarding the effectiveness of obesity prevention. The systematic and multidisciplinary design of the NHF-NRG programme enables the identification of potentially effective methods and strategies for the prevention of weight gain.

Adolescent↗
PubMed2005

Influence of beta(2)-adrenoceptor gene polymorphisms on diet-induced thermogenesis.

The sympathetic nervous system is involved in the control of energy metabolism and expenditure. Diet-induced thermogenesis is mediated partly by the ss-adrenergic component of this system. The aim of the present study was to investigate the role of genetic variation in the beta(2)-adrenoceptor in diet-induced thermogenesis. Data from twenty-four subjects (fourteen men and ten women; BMI 26.7(sem 0.8) kg/m(2); age 45.2(sem1.4) years) with different polymorphisms of the beta(2)-adrenoceptor at codon 16 (Gly16Gly, Gly16Arg or Arg16Arg) were recruited for this study. Subjects were given a high-carbohydrate liquid meal, and the energy expenditure, respiratory exchange ratio, and plasma concentrations of NEFA, glycerol, glucose, insulin and catecholamines were measured before and over 4 h after the meal. The AUC of energy expenditure (diet-induced thermogenesis) was not significantly different between polymorphism groups, nor was the response of any of the other measured variables to the meal. In a multiple regression model, the only variable that explained a significant proportion (32 %) of the variation in diet-induced thermogenesis was the increase in plasma adrenaline in response to the meal (P<0.05). The beta(2)-adrenoceptor codon16 polymorphisms did not contribute significantly. In conclusion, an independent contribution of the codon 16 polymorphism of the beta(2)-adrenoceptor gene to the variation in thermogenic response to a high-carbohydrate meal could not be demonstrated. The interindividual variation in thermogenic response to the meal was correlated with variations in the plasma adrenaline response to the meal.

Adipose Tissue↗