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Biomedical subjects

K J Acheson

Publications and source records attributed to K J Acheson.

At least 19 recordsLinked to original sources
PubMed2006

Changes of gut microbiota and immune markers during the complementary feeding period in healthy breast-fed infants.

INTRODUCTION: Little is known about changes in intestinal microbiota during the important period of complementary feeding (weaning). This descriptive study investigated changes of selected gut microbiota and markers of gut permeability and the immune system in breast fed infants during the complementary feeding period. METHODS: 22 healthy, exclusively breast fed infants (from birth to 4 months) with no antibiotic intake during the month prior to the study, were followed from 4 to 9 months of age. Faecal and saliva samples were collected at the start of the study (V0) and at monthly intervals (V1-V5) for measurement of selective gut microbiota (bifidobacteria, lactobacilli, vancomycin-insensitive lactobacilli, enterobacteria, enterococci, Clostridium perfringens) using semi-selective media. Immune markers (alpha-1-antitrypsin, eosinophil cationic protein (ECP), secretory IgA and TNF-alpha were measured in saliva and secretory IgA and TNF-alpha in faecal samples. RESULTS: High stool bifidobacteria counts at the start of the study (7.99 1 1.95 log10 CFU/g faeces) remained stable throughout the 5 months of complementary feeding while counts of enterobacteria and enterococci increased with age (P < 0.05 and P = 0.02 respectively). Vancomycin-insensitive lactobacilli increased significantly during weaning for V0 to V3 (P < 0.01), and then decreased slightly (V4). Faecal Clostridium perfringens remained below the detection limit during the study and parameters measured in saliva did not change. Faecal ECP decreased significantly from 1.011.4 (V0) to 0.510.9 mg/mg protein (V5) P = 0.03. CONCLUSION: Age and/or diet modifications during complementary feeding had no impact on faecal bifidobacteria counts but increased those of enterobacteria and enterococci. Transient increases in faecal lactobacilli and vancomycin-insensitive lactobacilli counts were observed. The reduction in faecal ECP may indicate a decrease in gut permeability (reinforcement of gut mucosa integrity) during the weaning period with age [corrected]

Biomarkers↗
PubMed2002

Severe underreporting of energy intake in normal weight subjects: use of an appropriate standard and relation to restrained eating.

OBJECTIVE: To assess the influence of different standards and restrained eating on underreporting in healthy, non-obese, weight-stable young subjects. DESIGN AND SUBJECTS: Eighty-three young adults (20-38 years, 55 women, 28 men) were assessed under weight-stable conditions with a 7-day dietary record and the three-factor eating questionnaire by Stunkard and Messick. Resting energy expenditure (REE; indirect calorimetry) plus data derived from physical activity records (PA) (Standard 1) or REE times an activity factor (AF) (Standard 2) was used as standard for total energy expenditure (TEE). For comparison, doubly labelled water (DLW) was used to measure TEE in a subgroup of subjects. RESULTS: There was an association between self-reported energy intake and Standard 2 but not with Standard 1. When compared with DLW both calculated standards were inaccurate, but Standard 2 avoided high levels of overreporting. Using Standard 2 to identify 'severe' underreporting (SU; as defined by a deviation of energy intake (EI) and TEE of >20%), SU was seen in 37% of all subjects. It was more frequently found in women than in men (49% of women, 14.3% of men, ). Underreporting subjects had a reduced EI but there were no significant differences in nutritional status (body weight and height, body mass index, fat mass and fat-free mass), energy expenditure and the proportion of energy from macronutrients between normal and underreporting subjects. However, high restraint was associated with a higher degree of underreporting in the total group, whereas disinhibition had an influence only in men. CONCLUSIONS: A high prevalence of SU is seen in non-obese subjects. Characteristics of eating behaviour (restraint and disinhibition) were associated with underreporting but seemed to have a different influence in men and women.

Adult↗
PubMed1998

Energy and substrate metabolism during a 42-day bed-rest in a head-down tilt position in humans.

Microgravity-induced changes in body composition (decrease in muscle mass and increase in fat mass) and energy metabolism were studied in seven healthy male subjects during a 42-day bed-rest in a head-down tilt (HDT) position. Resting energy expenditure (REE), fat and glucose oxidation were estimated by indirect calorimetry on days 0, +8 and +40 of the HDT period. Assessments were performed both in post-absorptive conditions and following two identical test meals given at 3-h intervals. Body composition (dual x-ray absorptiometry) was measured on days 0, +27, +42. Mean post-absorptive lipid oxidation decreased from 53 (SEM 8) mg x min(-1) (day 0) to 32 (SEM 10) mg x min(-1) (day 8, P = 0.04) and 36 (SEM 8) mg x min(-1) (day 40, P = 0.06). Mean post-absorptive glucose oxidation rose from 126 (SEM 15) mg x min(-1) (day 0) to 164 (SEM 14) mg x min(-1) (day 8, P = 0.04) and 160 (SEM 20) mg x min(-1) (day 40, P = 0.07). Mean fat-free mass (FFM) decreased between days 0 and 42 [58.0 (SEM 1.8) kg and 55.3 (SEM 1.7) kg, P < 0.01] while fat mass increased without reaching statistical significance. The mean REE decreased from 1688 (SEM 50) kcal x day(-1) to 1589 (SEM 42) kcal x day(-1) (P = 0.056). Changes in REE were accounted for by changes in FFM. Mean energy intake decreased from 2532 (SEM 43) kcal x day(-1) to 2237 (SEM 50) kcal x day(-1) (day 40, P < 0.01) with only a minor decrease in the proportion of fat. We concluded that changes in fat oxidation at the whole body level can be found during HDT experiments. These changes were related to the decrease in FFM and could have promoted positive fat balance hence an increase in fat mass.

Adult↗
PubMed1998

Energy expenditure of Chinese infants in Guangdong Province, south China, determined with use of the doubly labeled water method.

The doubly labeled water method was used to measure the energy expenditure of a group of 41, 4- or 6-mo-old infants with a cross-sectional design. The infants were divided into two groups according to whether they were breast-fed (11 at 4 mo, 9 at 6 mo) or formula fed (11 at 4 mo, 10 at 6 mo). Anthropometric measurements were recorded at birth and at the beginning and end of the 8-d study. Anthropometric data, which were supported by the food intake and energy expenditure results, indicated that the infants were within the norms for European and American infants of the same age. Mean energy intakes of 352 kJ (84 kcal) kg(-1) x d(-1) at 4 and 6 mo were lower than the FAO/WHO/UNU recommended value of 452 kJ (108 kcal) x kg(-1) x d(-1)) and Chinese recommendations of 502 kJ (120 kcal) kg(-1) x d(-1). However, some authors believe that values of 398 kJ (95 kcal) kg(-1) x d(-1) at 4 mo and 356 kJ (85 kcal) kg(-1) x d(-1) at 6 mo are more appropriate. At 6 mo the infants' length-for-age and weight-for-age were at the National Center for Health Statistics 55th and 47th percentiles, respectively, whereas 58% were below the 50th percentile for weight-for-length. We conclude that at 4 mo infants receive sufficient energy for their requirements. However, at 6 mo energy requirements might well be greater than the revised recommendations, when infants are being weaned to alternative foods and are more prone to the influence of diet on their growth and development.

Anthropometry↗
PubMed1995

Energy, protein, and substrate metabolism in simulated microgravity.

Whole body protein turnover and energy expenditure before and during an oral glucose tolerance test (1 g/kg body wt) were studied on separate occasions in six healthy young men before and during 3 days of simulated microgravity using the 6 degrees head-down tilt (HDT) method. After 42-47 h of HDT, basal insulin concentrations increased significantly from 9.4 +/- 1.9 to 13.1 +/- 0.1 microU/ml (P < 0.002). No significant differences in glycemia, insulinemia, or free fatty acid concentrations were observed in response to the oral glucose load. With HDT, increases were observed in basal postabsorptive resting metabolic rate (8%; P < 0.05), lipid oxidation (33 +/- 2 to 51 +/- 5 mg/min; P < 0.02), and the thermic effect of glucose (7.7 +/- 1 to 10.7 +/- 0.6%; not significant). Protein turnover (arithmetic mean of ammonia and urea flux rates) was unchanged by HDT, but a significant increase was seen when calculated from ammonia alone (P < 0.02). The present data show that HDT results in an increased energy requirement through elevations in both the basal metabolic rate and the thermic response to food ingestion. These changes may have been brought about by a cephalic shift of body fluids similar to that experienced in microgravity.

Administration, Oral↗
PubMed1992

Thermic effect of epinephrine: a role for endogenous insulin.

The contribution of the basal insulin concentration to the metabolic response to epinephrine was measured in eight, postabsorptive, healthy volunteers before and during epinephrine (0.05 micrograms/kg fat-free mass [FFM] x min) and somatostatin (500 micrograms/h) infusion with and without insulin (0.1 mU/kg body weight [BW] x min) replacement. At basal plasma insulin concentrations, epinephrine increased oxygen consumption, heart rate, heart work, hepatic glucose production, glycogen breakdown in liver and muscle, and glucose oxidation, and the arterial plasma concentrations of glucose, lactate, and free fatty acids. Similar effects were observed during hypoinsulinemia, but epinephrine's actions on oxygen consumption and plasma concentrations of free fatty acids were disproportionally enhanced. We conclude that epinephrine-induced thermogenesis is partially inhibited by basal plasma insulin concentrations.

Adult↗
PubMed1992

Thermogenesis and fructose metabolism in humans.

Resting metabolic rate was measured in 10 healthy volunteers (25 yr, 73 kg, 182 cm) for 1 h before and 4 h during intravenous (iv) fructose administration (20% at 50 mumol.kg-1.min-1) with (+P) or without (-P) propranolol (100 micrograms/kg, 1 microgram.kg-1.min-1) during the last 2 h. Some subjects were studied a further 2 h with fructose infusion and +P or -P in hyperinsulinemic (2.9 pmol.kg-1.min-1) euglycemic conditions. Glucose turnover ([3-3H]glucose, 20 muCi bolus and 0.2 muCi/min) was calculated over 30 min at 0, 2, 4, and 6 h. The thermic effect of iv fructose was approximately 7.5% and decreased to 4.9 +/- 0.4% (P less than 0.01) +P. During the euglycemic clamp the thermic effect was 6.2 +/- 0.9% (-P) and 5.3 +/- 0.9% (+P). Hepatic glucose production (HGP) was 11.7 mumol.kg-1.min-1 (0 h) and did not change after 2 h iv fructose (11.8 +/- 0.5 and 9.8 +/- 0.6 mumol.kg-1.min-1 -P and +P, respectively) but increased to 13.8 +/- 0.9 (-P) and 12.9 +/- 0.8 mumol.kg-1.min-1 (+P) (P less than 0.01) after 4 h. HGP was suppressed to varying degrees during the euglycemic clamp. It is concluded that 1) the greater thermic effect of fructose compared with glucose is probably due to continued gluconeogenesis (which is suppressed by glucose or glucose-insulin) and the energy cost of fructose metabolism to glucose in the liver. 2) There is a sympathetically mediated component to the thermic effect of fructose (approximately 30%) that is not mediated by elevated plasma insulin concentrations similar to those observed with iv glucose.

Adrenergic beta-Antagonists↗
PubMed1990

Evidence that hyperglycaemia per se does not inhibit hepatic glucose production in man.

The effect of hyperglycaemia on hepatic glucose production (Ra) was investigated in nine healthy men using sequential clamp protocols during somatostatin infusion and euglycaemia (0-150 min), at plasma glucose levels of 165 mg x dl-1 (9.2 mM, 150-270 min) and during insulin infusion (1.0 mU x kg-1 x min-1, 270-360 min) in study 1 or during hypo-insulinaemia and plasma glucose levels of 220 mg x dl-1 (12.2 mM; 270-390 min) in study 2. Somatostatin decreased Ra and glucose disposal rate (Rd) but increased plasma free fatty acids (FFA) and lipid oxidation during euglycaemia. Increasing plasma glucose to 165 mg x dl-1 (9.2 mM) and hypo-insulinaemia increased Rd, but no suppressive effects on Ra, plasma FFA and lipid oxidation were observed. By contrast hyperinsulinaemia (study 1), as well as a further increase in plasma glucose (study 2), both decreased Ra. However, more pronounced hyperglycaemia increased insulin secretion despite somatostatin resulting in a fall in plasma FFA and lipid oxidation. Our data questions the accepted dogma that hyperglycaemia inhibits Ra independently of insulin action.

Adult↗
PubMed1990

Thyroid hormone action on lipid metabolism in humans: a role for endogenous insulin.

The effects of moderate hyperthyroidism on lipid metabolism were investigated in six healthy subjects before and after thyroxine treatment (300 micrograms/d). T4-treatment increased basal metabolic rate (+8%) and glucose oxidation (+87%), without affecting lipid oxidation, plasma free fatty acids, glycerol, and beta-hydroxybutyrate. During euthyroidism, a hypoinsulinaemic-euglycaemic 150-minute clamp protocol increased energy expenditure (+3%), lipid oxidation (+42%), plasma free fatty acids (+254%), glycerol (+232%), and beta-hydroxybutyrate (+343%), but decreased glucose oxidation (-20%). Similar effects were observed after T4-treatment, but hyperthyroidism induced disproportionate increases in energy expenditure (+7%), plasma glycerol (+310%), and ketone body levels (+436%). We conclude that moderate hyperthyroidism enhances hypoinsulinemia-induced increases in lipolysis, free fatty acid recycling, and ketogenesis without affecting lipid oxidation. Thus basal insulin may camouflage some of thyroid hormone action on lipid metabolism.

3-Hydroxybutyric Acid↗
PubMed1990

Thermogenic effect of thyroid hormones: interactions with epinephrine and insulin.

The interactions between thyroid hormones, epinephrine, and insulin in the regulation of energy expenditure were investigated in a group of healthy young men before and after thyroxine (T4) treatment (300 micrograms/day for 14 days) at basal plasma insulin concentrations and during hypoinsulinemia with and without epinephrine infusion (0.05 micrograms.kg fat-free mass-1.min-1). T4 treatment induced moderate hyperthyroidism and increased resting energy expenditure (RMR). The effect was more pronounced during short-term hypoinsulinemia, but hypoinsulinemia by itself did not influence RMR. Epinephrine infusion caused a significant increase in energy expenditure. The effect was most pronounced at hypoinsulinemia and with T4 treatment. Hypoinsulinemia and T4 treatment were not additive in their effects. We conclude that basal insulin concentrations mask some of the thermogenic effects of thyroid hormones and epinephrine. Thus insulin antagonism may suppress some of the thermogenic actions of thyroid hormones and epinephrine.

Adult↗
PubMed1989

The parasympathetic nervous system and the thermic effect of glucose/insulin infusions in humans.

The thermic effect of glucose/insulin infusions was investigated in seven healthy young men before and during either inhibition (atropine sulphate 10 micrograms/kg bolus; 10 micrograms/kg/h) or stimulation (edrophonium chloride, 10 mg bolus; 0.75 mg/min starting rate) of the parasympathetic nervous system. The thermic effects of glucose/insulin were 6.2% +/- 0.4% and 5.6% +/- 0.7% before atropine and edrophonium, respectively, and increased to 7.1% +/- 0.5% (NS) with atropine and 7.5% +/- 1.2% (P less than .05) with edrophonium. In four subjects atropine or edrophonium was infused before the hyperinsulinemic, euglycemic clamp. A significant increase in resting metabolic rate and plasma norepinephrine concentrations was observed with edrophonium alone. When the thermic effects of glucose/insulin were calculated with respect to the metabolic rates observed during the drug infusions alone, they were 5.9% +/- 1.4% and 3.6% +/- 0.6% (NS) for the clamp + atropine and clamp + edrophonium, respectively. These results demonstrate that the increases in the thermic effect of glucose/insulin infusions observed during inhibition or stimulation of the parasympathetic nervous system were due to atropine or edrophonium increasing the resting metabolic rate rather than increasing the thermic response to glucose-insulin infusions. However, because it has been shown that atropine can decrease the thermic effect of an orally administered meal by approximately 60%, it would appear that the parasympathetic nervous system can influence the thermic effect of food by affecting the rate of digestion, absorption and storage of the ingested nutrients.

Adult↗
PubMed1989

Thermogenesis in men and women induced by fructose vs glucose added to a meal.

Energy expenditure (EE) was measured by indirect calorimetry in 20 subjects (10 men and 10 women) for 30 min before and 6 h after the ingestion of a mixed meal containing 20% protein, 33% fat, and either 75 g glucose or 75 g fructose as carbohydrate source (47%). Diet-induced thermogenesis (DIT) and the rate of carbohydrate oxidation were significantly greater with fructose (12.4 +/- 0.6% and 54.8 +/- 2.1 g/6 h, respectively) than with glucose (10.7 +/- 0.7%, p less than 0.01, and 48.3 +/- 2.4 g/6 h, p less than 0.01, respectively). The DIT of male (12.1 +/- 1% and 13.9 +/- 0.8% with glucose and fructose, respectively) was greater than that of female subjects (9.2 +/- 0.7%, p less than 0.05, and 11.0 +/- 0.7%, p less than 0.05, respectively). In contrast to the glucose meal, negligible changes in plasma levels of glucose and insulin were observed with the fructose meal but plasma levels of lactate increased more with fructose than with glucose (peak values: 3.3 +/- 0.6 vs 1.5 +/- 0.1 mmol/L, respectively). When fructose provides the only carbohydrate source of a mixed meal, it induces a larger increase in carbohydrate oxidation and thermogenesis than when glucose is the carbohydrate source.

Adolescent↗
PubMed1989

Glucoregulatory function of thyroid hormones: role of pancreatic hormones.

Glucose metabolism was investigated in humans before and 14 days after 300 micrograms L-thyroxine (T4)/day using a sequential clamp protocol during short-term somatostatin infusion (500 micrograms/h, 0-6 h) at euglycemia (0-2.5 h), at 165 mg/dl (2.5-6 h), and during insulin infusion (1.0 mU.kg-1.min-1, 4.5-6 h). T4 treatment increased plasma T4 (+96%) and 3,5,3'-triiodothyronine (T3, +50%), energy expenditure (+8%), glucose turnover (+32%), and glucose oxidation (Glucox +87%) but decreased thyroid-stimulating hormone (-96%) and nonoxidative glucose metabolism (Glucnonox, -30%) at unchanged lipid oxidation (Lipox). During somatostatin and euglycemia glucose production (Ra, -67%) and disposal (Rd, -28%) both decreased in euthyroid subjects but remained at -22% and -5%, respectively, after T4 treatment. Glucox (control, -20%; +T4, -25%) fell and Lipox increased (control, +42%; +T4, +45%) in both groups, whereas Glucnonox decreased before (-36%) but increased after T4 (+57%). During somatostatin infusion and hyperglycemia Rd (control, +144%; +T4, +84%) and Glucnonox (control, +326%; +T4, +233%) increased, whereas Glucox and Lipox remained unchanged. Insulin further increased Rd (+76%), Glucox (+155%), and Glucnonox (+50%) but decreased Ra (-43%) and Lipox (-43%). All these effects were enhanced by T4 (Rd, +38%; Glucox, +45%; Glucnonox, +35%; Ra, +40%; Lipox, +11%). Our data provide evidence that, in humans, T3 stimulates Ra and Rd, which is in part independent of pancreatic hormones.

Adult↗
PubMed1988

Two-week stimulation or blockade of the sympathetic nervous system in man: influence on body weight, body composition, and twenty four-hour energy expenditure.

Seven lean healthy young men were studied for 6 weeks during exposure to pharmacologic inhibition or stimulation of the sympathetic nervous system. For a period of 2 weeks their beta-adrenergic receptors were either blocked with propranolol hydrochloride (160 mg/d) or stimulated with terbutaline sulphate (15 mg/d). After a further 2 weeks of placebo administration (500 mg lactose/d), the subjects crossed over to the drug they had not been taking at the beginning of the experiment for another 14 days. During the last five days of each 2-week period, the subjects consumed a weight-maintaining diet, composed of 12% protein, 48% carbohydrate, and 40% fat. They consumed exactly the same menus on the same days during the subsequent study periods. Body weight and physical activity were measured every day for 6 weeks. Daily heart rate and nitrogen excretion were measured continuously for days at the end of each 2-week period, the last two days of which were spent in a respiration chamber where energy expenditure and a variety of metabolic parameters were measured. In the respiration chamber on the propranolol, placebo, and terbutaline treatments, respectively, significant differences were observed in mean daily heart rate (65 +/- 3, 75 +/- 4, and 84 +/- 4 beats/min), mean sleeping heart rate (51 +/- 2, 56 +/- 3, and 62 +/- 3 beats/min), nitrogen excretion (13.6 +/- 0.7, 12.6 +/- 0.6, and 11.9 +/- 0.6 g/d), fat oxidation (+1,045 +/- 95, +1,243 +/- 148, and +1,278 +/- 84 kcal/d) and thyroid hormones (12.0 +/- 0.7, 15.7 +/- 0.9, and 17.2 +/- 1.0 T3/T4 ratio).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Glycogen storage capacity and de novo lipogenesis during massive carbohydrate overfeeding in man.

The metabolic balance method was performed on three men to investigate the fate of large excesses of carbohydrate. Glycogen stores, which were first depleted by diet (3 d, 8.35 +/- 0.27 MJ [1994 +/- 65 kcal] decreasing to 5.70 +/- 1.03 MJ [1361 +/- 247 kcal], 15% protein, 75% fat, 10% carbohydrate) and exercise, were repleted during 7 d carbohydrate overfeeding (11% protein, 3% fat, and 86% carbohydrate) providing 15.25 +/- 1.10 MJ (3642 +/- 263 kcal) on the first day, increasing progressively to 20.64 +/- 1.30 MJ (4930 +/- 311 kcal) on the last day of overfeeding. Glycogen depletion was again accomplished with 2 d of carbohydrate restriction (2.52 MJ/d [602 kcal/d], 85% protein, and 15% fat). Glycogen storage capacity in man is approximately 15 g/kg body weight and can accommodate a gain of approximately 500 g before net lipid synthesis contributes to increasing body fat mass. When the glycogen stores are saturated, massive intakes of carbohydrate are disposed of by high carbohydrate-oxidation rates and substantial de novo lipid synthesis (150 g lipid/d using approximately 475 g CHO/d) without postabsorptive hyperglycemia.

Adult↗
PubMed1988

Effect of thyroid hormones on oxidative and nonoxidative glucose metabolism in humans.

The glucoregulatory function of thyroid hormones was investigated in six healthy subjects before and after 14 day 3,5,3',5'-tetraiodothyronine (T4) treatment (300 micrograms/day) using a sequential clamp protocol for 5 h at euglycemia (0-2 h) and hyperglycemia (165 mg/dl, 2-5 h) and different insulin infusion rates (1.0 for 0-3.5 h and 6.5 mU.kg-1.min-1, for 3.5-5 h). T4 treatment increased basal energy expenditure (+8%), glucose disposal (+31%), and oxidation (+87%) but decreased nonoxidative glucose metabolism (-30%) and was without effect on lipid oxidation. During the euglycemic clamp, T4 treatment enhanced insulin-induced glucose disposal (+16%), glucose oxidation (+34%), and inhibition of lipid oxidation (-66 vs. -40%); nonoxidative glucose metabolism was stimulated to a similar extent before and after T4. During hyperglycemia, 3,5,3'-triiodothyronine (T3) did not affect glucose disposal but increased carbohydrate-induced lipogenesis at both insulin infusion rates. We conclude that T4 treatment promotes glucose disposal and oxidation, T3 decreases noninsulin-mediated glucose storage but does not antagonize insulin action.

Adult↗
PubMed1987

Carbohydrate metabolism and de novo lipogenesis in human obesity.

Respiratory exchange was measured during 14 consecutive hours in six lean and six obese individuals after ingestion of 500 g of dextrin maltose to investigate and compare their capacity for net de novo lipogenesis. After ingestion of the carbohydrate load, metabolic rates rose similarly in both groups but fell earlier and more rapidly in the obese. RQs also rose rapidly and remained in the range of 0.95 to 1.00 for approximately 8 h in both groups. During this time, RQ exceeded 1.00 for only short periods of time with the result that 4 +/- 1 g and 5 +/- 3 g (NS) of fat were synthesized via de novo lipogenesis in excess of concomitant fat oxidation in the lean and obese subjects, respectively. Results demonstrate that net de novo lipid synthesis from an unusually large carbohydrate load is not greater in obese than in lean individuals.

Adult↗