Empathy is important for enablement.
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Empathy↗
Biomedical subjects
S W Mercer
Publications and source records attributed to S W Mercer.
A qualitative study of general practitioners' and practice nurses' attitudes to obesity management in primary care.
OBJECTIVES: To examine general practitioners' (GPs) and practice nurses' (PNs) perceptions of obesity, their strategies and attitudes towards weight management, and their views on the major obstacles to (and need for) better weight management in primary care. METHOD: A qualitative study was carried out using semi-structured interviews with GPs and PNS within the Greater Glasgow Healthboard area. RESULTS: GPs and PNs understood the problem of obesity but generally had little enthusiasm for weight management. Most of the GPs felt it was an inappropriate use of their time and passed obese patients onto the PNs; the PNs felt that obese patients were "off-loaded" onto them. Stated management objectives were aimed at "healthy lifestyle" rather than "unrealistic" weight loss, yet frustration at "lack of success" was a major theme. Lack of motivation on the part of the patient was seen as the major problem. GPs were keener to be directly involved when a concomitant disease was present. Suggested requirements to improve weight management at the level of primary care included more time, better facilities, community dieticians and more training courses. However, many felt that Government, media and public health had to take a leading role in order to deal with the problem effectively. CONCLUSIONS: A comprehensive and integrative primary care-led approach to weight management may be possible but will need substantial shifts of resources, organisation, training and attitudes in order to maximise its potential impact.
Attitude of Health Personnel↗
The development of resistance to the lipogenic effects of insulin in brown and white adipose tissue of spontaneously type II diabetic male CBA/Ca mice.
1. Lipogenesis in brown adipose tissue and white adipose tissue (WAT) was measured in vivo in spontaneously type II diabetic male CBA/Ca mice. 2. Lipogenic rates rose sharply in brown adipose tissue between the third and fourth month of life, concomitant with the onset of hyperinsulinaemia. However, lipogenic rates fell between the fourth and fifth month of age, and remained low, despite increasing circulating insulin concentrations. 3. Lipogenesis in white adipose tissue showed a modest response to hyperinsulinaemia followed by increasing resistance to elevated insulin concentrations after 5 months of age. 4. Studies involving either the injection of insulin or the intubation of glucose provided further evidence for the development of insulin resistance in both brown and white adipose tissue.
Adipose Tissue↗
Rapid inhibition by intragastric triolein of the re-activation of glucose utilization and lipogenesis in the mammary gland during the starved-refed transition in lactating rats. Evidence for a direct effect of oral lipid on mammary tissue.
1. Oral administration of triacylglycerol (triolein) to starved/chow-refed lactating rats suppressed the lipogenic switch-on in the mammary gland in vivo. 2. A time-course study revealed that triolein, administered at 30 min after the onset of refeeding, had no influence on lipogenic rate in the mammary gland between 30 and 60 min, but markedly decreased it between 60 and 90 min. Glucose uptake by the mammary gland (arteriovenous difference) increased by 30 min of refeeding, as did lactate production. Between 30 and 90 min glucose uptake remained high in the control animals, but glucose uptake and net C3-unit uptake were decreased in the triolein-loaded animals by 90 min. 3. Triolein increased [glucose 6-phosphate] in the gland and simultaneously decreased [fructose 1,6-bisphosphate], indicative of a decrease in phosphofructokinase activity. This cross-over occurred at 60 min, i.e. immediately before the inhibition of lipogenesis, and by 90 min had reached 'starved' values. 4. Triolein had no effect on plasma [insulin] nor on whole-blood [glucose], [lactate] or [3-hydroxybutyrate]; a small increase in [acetoacetate] was observed. 5. Infusion of the lipoprotein lipase inhibitor, Triton WR1339, abolished the suppression of mammary-gland lipogenesis by triolein and the increase in the [glucose 6-phosphate]/[fructose 1,6-bisphosphate] ratio, suggesting a direct influence of dietary lipid on mammary-gland glucose utilization and phosphofructokinase activity.
Animals↗
The influence of starvation and natural refeeding on the rate of triacylglycerol/fatty acid substrate cycling in brown adipose tissue and different white adipose sites of the rat in vivo. The role of insulin and the sympathetic nervous system.
Triacylglycerol/fatty acid substrate cycling was measured in vivo in brown adipose tissue (BAT) and white adipose tissue (WAT) of fed, starved and refed rats. Starvation (24h) significantly decreased the rate of cycling in BAT, and refeeding chow diet led to a rapid, 6-fold increase in cycling. Cycling rate in WAT was much lower than in BAT, and was not influenced by fasting or refeeding. Similar rates of cycling were found in epididymal, mesenteric, subcutaneous, and scapular WAT depots. Sympathetic denervation of interscapular BAT abolished the response of the tissue to refeeding, as did acute suppression of insulin secretion. Similarly, rats fasted for 3 days showed no acute increase in the activity of the cycle following refeeding.
Adipose Tissue↗
The regulation of lipogenesis in vivo in the lactating mammary gland of the rat during the starved-refed transition. Studies wtih acarbose, a glucosidase inhibitor.
Depression of carbohydrate digestion by oral administration of acarbose, a glucosidase inhibitor, led to a 75% inhibition of the re-activation of lipogenesis in vivo in the mammary gland of 18 h-starved lactating rats refed with 5 g of chow diet. Rates of [1-14C]glucose incorporation in vitro into lipid and CO2 in mammary-gland acini isolated from refed animals were elevated compared with acini from starved rats, but acarbose treatment completely prevented this stimulation. Gastric intubation of glucose led to a large stimulation of lipogenesis in the mammary gland of starved lactating rats, similar to that induced by refeeding with chow diet; this was dependent on the amount of glucose given and the time elapsed between glucose administration and injection of 3H2O for the measurement of lipogenesis. The switch-on of lipogenesis in the mammary gland of starved lactating rats, by refeeding or by intubation of glucose, was associated with a decrease in the ratio of [glucose 6-phosphate]/[fructose 1,6-bisphosphate] in the gland, indicative of an increase in phosphofructokinase activity. A time-course study revealed that the ratio decreased rapidly over the first 30 min of chow refeeding, after which a large surge in lipogenesis was seen. Acarbose, given 25 min after the onset of refeeding, led to a stepwise increase in the ratio, in parallel with the observed decrease in lipogenic activity. It is concluded that the control of lipogenesis in the mammary gland is closely linked to the availability of dietary carbohydrate. An important site of regulation of lipogenesis in the gland appears to be at the level of phosphofructokinase. A possible role of insulin in the regulation of phosphofructokinase activity, and the acute modulation of insulin-sensitivity in the gland during the starved-refed transition, are discussed.
Acarbose↗
Effect of high fat diets on energy balance and thermogenesis in brown adipose tissue of lean and genetically obese ob/ob mice.
The effects on energy balance and brown adipose tissue thermogenesis of feeding high fat diets of differing fatty acid composition have been investigated in lean and genetically obese (ob/ob) mice. Groups of mice were fed either a low fat diet or a high fat diet based on corn oil or beef tallow for 2 wk. Energy intake and body weight gain were higher in both lean and obese animals fed the high fat diets than in respective mice fed the low fat diets. Carcass energy gain was greater for the obese than for the lean consuming each of the diets. Both lean and obese mice had a higher energy gain when fed the beef tallow diet than when fed the corn oil, despite isoenergetic intakes of the two diets. The thermogenic activity of brown adipose tissue, assessed from measurements of cytochrome oxidase activity and mitochondrial guanosine 5'-diphosphate (GDP) binding, were greater in both lean and obese mice fed the corn oil diet than in those fed the low fat diet. However, GDP binding and cytochrome oxidase activities in lean or obese mice fed the beef tallow diet were not different from those of mice of the same genotype fed the low fat diet. These results indicate that in both lean and obese (ob/ob) mice energy deposition and the stimulation of brown adipose tissue thermogenesis during the voluntary hyperphagia induced by feeding high fat diets are influenced by the fatty acid composition of the diet. A diet rich in polyunsaturated fatty acids appears to result in preferential stimulation of the thermogenic activity of brown adipose tissue, particularly in the ob/ob mouse.
Adipose Tissue, Brown↗
Time course of changes in plasma glucose and insulin concentrations and mammary-gland lipogenesis during re-feeding of starved conscious lactating rats.
Temporal changes in circulating insulin concentrations were measured during re-feeding of 18 h-starved lactating rats. Insulin concentrations rose rapidly over the first 20 min of re-feeding with 5 g of chow diet, and then sharply declined between 20-30 min and remained low for the rest of the 90 min experimental period. Lipogenic activity in the mammary gland also exhibited a peak during re-feeding, but there was a clear time lag between the insulin response and the lipogenic response. Blood-flow measurements failed to show any major increase to the tissue during this activation of lipogenesis. Acute suppression of insulin secretion at 30 min (after the initial surge) abolished the switch-on of lipogenesis, suggesting that the insulin-sensitivity of the gland may be acutely enhanced over this period of re-feeding.
Animals↗
Effects of ciglitazone on insulin resistance and thermogenic responsiveness to acute cold in brown adipose tissue of genetically obese (ob/ob) mice.
Genetically obese (ob/ob) mice develop a marked insulin resistance in brown adipose tissue soon after weaning, and this is paralleled by a fall in the acute activation of the mitochondrial proton conductance pathway in the tissue on cold exposure. Treatment of ob/ob mice with ciglitazone, a new oral hypoglycaemic, led to a restoration of insulin sensitivity in brown adipose tissue. The amelioration of insulin resistance was accompanied by a normalization of the acute, cold-induced increase in mitochondrial GDP binding. These results support the hypothesis that the development of insulin resistance in brown adipose tissue is an important factor in the impaired thermogenic responsiveness of obese mice.
Adipose Tissue, Brown↗
Brown adipose tissue thermogenesis in obese animals.
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Adipose Tissue, Brown↗
The development of insulin resistance in brown adipose tissue may impair the acute cold-induced activation of thermogenesis in genetically obese (ob/ob) mice.
Genetically obese (ob/ob) mice develop insulin resistance in brown adipose tissue during the fifth week of life. Prior to this, at 26 days of age, ob/ob mice show a substantial increase in GDP binding to brown-adipose-tissue mitochondria during acute cold exposure. When insulin resistance in brown fat develops, by 35 days of age, the increase in GDP binding in response to cold is markedly reduced. Studies with 2-deoxyglucose suggest that insulin resistance in brown adipose tissue could impair thermogenic responsiveness during acute cold exposure by limiting the ability of the tissue to take up glucose.
Adipose Tissue, Brown↗
Effect of high fat diets on the thermogenic activity of brown adipose tissue in cold-acclimated mice.
The effects of feeding high fat diets on thermogenesis in brown adipose tissue has been investigated in cold-acclimated mice. Two high fat diets of differing fatty acid composition were used, one of which was based on corn oil and the other on beef tallow. After 3 weeks of feeding the diets there was little difference in the weight, protein content and cytochrome oxidase activity of brown adipose tissue (interscapular plus subscapular) of mice fed the high fat diets from those given the low fat stock diet. However, the mice fed the high fat diets showed marked increases in mitochondrial GDP binding and in mitochondrial respiration, consistent with an augmentation in the activity of the proton conductance pathway. This increase in thermogenesis in brown adipose tissue mitochondria occurred without any elevation in digestible energy intake, and is therefore not a response to overfeeding. It is concluded that the activity of the proton conductance pathway in brown adipose tissue of cold-acclimated mice can be modulated by the level of dietary triglyceride independently of energy intake. We suggest that the effect of high fat diets on thermogenesis in brown adipose tissue may relate to the suppressive effects of dietary lipid on fatty acid synthesis in the tissue.
Acclimatization↗
Developmental changes in fatty acid synthesis in interscapular brown adipose tissue of lean and genetically obese (ob/ob) mice.
Fatty acid synthesis was measured in vivo with 3H2O in interscapular brown adipose tissue of lean and genetically obese (ob/ob) mice. At 26 days of age, before the development of hyperphagia, synthesis in brown adipose tissue was higher in the obese than in the lean mice; synthesis was also elevated in the liver, white adipose tissue and carcass of the obese mice. At 8 weeks of age, when hyperphagia was well established, synthesis remained elevated in all tissues of the obese mice, with the exception of brown adipose tissue. Elevated synthesis rates were not apparent in brown adipose tissue of the obese mice at 14 days of age, nor at 35 days of age. These results demonstrate that brown adipose tissue in ob/ob mice has a transitory hyperlipogenesis at, and just after, weaning on to a low-fat/high-carbohydrate diet. Once hyperphagia has developed, by week 5 of life, brown adipose tissue is the only major lipogenic tissue in the obese mice not to exhibit elevated rates of fatty acid synthesis; this suggests that insulin resistance develops much more rapidly in brown adipose tissue than in other lipogenic tissues of the ob/ob mouse.
Adipose Tissue, Brown↗