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Biomedical subjects

M Enser

Publications and source records attributed to M Enser.

34 records · Page 2Linked to original sources

Fatty acid composition of triglycerides from adipose tissue transplanted between obese and lean mice.

The subcutaneous adipose tissue of genetically obese mice (ob/ob) differs from that of lean littermates not only by virtue of its larger cells but also in its fatty acid composition; it contains a higher proportion of palmitoleic acid and a lower proportion of linoleic acid. To determine whether these differences in fatty acid composition were inherent in fat cells, subcutaneous adipose tissue from obese and lean mice was transplanted under the kidney capsules of lean and obese host mice and the fatty acid composition of the neutral lipids of the graft and of the host perirenal and subcutaneous fat was determined 1 or 2 months later. The fatty acid composition of grafts from lean donors in obese mice resembled that of the perirenal adipose tissue of the obese hosts after 1 month, with a lower proportion of linoleic acid and a higher proportion of palmitoleic acid than in lean mice. Grafts from obese mice in lean mice had fatty acid compositions which were either unchanged, partially changed or which completely resembled that of the host. The use of grafts prelabeled by feeding the donor margaric acid indicated that total lack of fatty acid turnover, rather than selective metabolic processes, was responsible for the failure of some grafts from obese mice in lean mice to acquire the fatty acid composition of the perirenal adipose tissue of the host.

Adipose Tissue↗

The actions of dichloroacetic acid on blood glucose, liver glycogen and fatty acid synthesis in obese-hyperglycaemic (ob/ob) and lean mice.

Obese-hyperglycaemic mice and lean mice were injected with dichloroacetate to determine the significance of gluconeogenesis in maintaining the hyperglycaemia of obese mice and to investigate the effects of a fall in blood glucose on fatty acid synthesis. One hour after the second of two, hourly, injections of dichloroacetate the blood glucose concentrations in fed and starved lean mice were decreased, whereas in obese mice they were sharply increased. In obese and lean mice, both fed and starved, dichloroacetate decreased plasma lactate but insulin was unchanged. The quantity of liver glycogen was decreased in all dichloroacetate treated mice, with the largest falls in fed and starved obese mice, which had much larger glycogen stores than lean mice. Dichloroacetate treatment decreased the concentration of plasma non-esterified fatty acids in fed and starved obese mice and fed lean mice but not in starved lean mice. Fatty acid synthesis in white (inguinal, subcutaneous) adipose tissue was stimulated by dichloroacetate in fed obese mice and inhibited in fed lean mice. Fatty acid synthesis in brown adipose tissue (scapular) was faster than in white adipose tissue and was less affected by dichloroacetate although the changes were in the same direction as in white adipose tissue. We attribute the increased hyperglycaemia of obese mice treated with dichloroacetate to increased glycogenolysis coupled with a failure to secrete additional insulin in response to the raised blood glucose. This high blood glucose concentration in dichloroacetate treated obese mice may in turn explain the increased fatty acid synthesis in their white adipose tissue.

Acetates↗

The regulation of hepatic stearoyl-coenzyme A desaturase in obese-hyperglycaemic (ob/ob) mice by food intake and the fatty acid composition of the diet.

1. The effects of food intake and the fatty acid composition of the diet on the hepatic stearoyl-CoA desaturase activity of obese-hyperglycaemic (ob/ob) mice were investigated. 2. Obese mice fed on a commercial mouse diet, ad libitum, had 6.5-fold more activity per liver cell than had lean mice. 3. On a diet containing 14% corn oil the activity was 65% less in obese mice and 62% less in lean mice compared with animals fed on the commercial diet. 4. Feeding with 14% saturated fat in the diet doubled the activity in lean mice compared with those on the commercial diet, but had no effect on the activity in obese mice. 5. Obese mice fed on the corn-oil diet contained a higher proportion of linoleic acid in the liver lipids than did lean mice fed on the commercial diet, but the acyl-CoA desaturase activity was 125% higher than in the lean mice. 6. Limiting the food intake of obese mice by pair-feeding with lean mice decreased their acyl-CoA desaturase activity when the animals were fed on the saturated-fat diet, but the activity remained 75% higher than in lean mice, whereas in obese mice pair-fed on the corn-oil diet the activity was the same as in lean mice. 7. During starvation the acyl-CoA desaturase activity in livers from obese mice decreased more slowly and proportionately less than in livers from lean mice. 8. It is concluded that increased substrate supply as a result of hyperphagia and not low concentration of linoleic acid is the main factor causing high acyl-CoA desaturase activity in obese mice.

Animals↗

The role of insulin in the regulation of stearic acid desaturase activity in liver and adipose tissue from obese--hyperglycaemic (ob/ob) and lean mice.

The relationship between the hyperinsulinaemia of obese--hyperglycaemic (ob/ob) mice and their high activity of stearic acid delta 9-desaturase compared with lean mice has been investigated. The concentrations of plasma insulin in obese mice were decreased by 71, 88 and 96% after treatment either with alloxan or food restriction to maintain the same weight as lean mice, or treatment of the weight restricted mice with alloxan followed by feeding ad libitum. The concentration of plasma insulin produced by the latter treatment was the same as in normal lean mice. After treatment the hepatic desaturase activities were 24, 68 and 19% less respectively on a cell basis than in livers from untreated obese mice, and the total epididymal fat-pad activities were lower by 16, 62 and 57%. These results suggest that hyperinsulinaemia is not essential for the increased hepatic desaturase, controlling the hepatic desaturase activity, but even this may be subject to overriding regulation by the concentration of esterified linoleic acid in the liver lipids, which was negatively correlated (r = 0.91, P less than 0.001) with desaturase activity.

Adipose Tissue↗

Desaturation of stearic acid by liver and adipose tissue from obese-hyperglycaemic mice (ob/ob).

Stearic acid desaturase activity was assayed in preparations from perigenital adipose tissue and liver from lean and genetically obese female mice (ob/ob). The total activity in the perigenital adipose tissue from obese mice was threefold greater than in the tissue from lean mice, but per g of adipose tissue the activity was twofold greater in tissue from lean mice. In liver, the activity in obese mice was elevated at 8 weeks of age, remained elevated up to 24 weeks and then decreased by half at 48 weeks, but at all ages was higher than that in lean mice. The decrease in desaturase activity of liver from obese mice at 48 weeks corresponded to a change in the fatty acid composition of liver lipids toward that found in lean mice. Whereas in adipose tissue much of the increased enzyme activity may be due to tissue hyperplasia, in liver it is mainly an increased activity per cell.

Adipose Tissue↗

Clearing-factor lipase in muscle and adipose tissue of pigs.

1. Clearing-factor lipase was assayed in acetone-ether-dried powders of heart and adipose tissue of pigs. The enzyme activity in heart was higher than that in adipose tissue. The activity in the outer layer of subcutaneous fat was greater than that in the inner subcutaneous fat and the perirenal fat, which had similar activities. 2. Starvation for 48h, but not for 24h, decreased the activity of the heart enzyme. 3. Starvation for 24h caused a rapid decrease in the activity in all three adipose tissues, but even after 72h of starvation the activity was still highest in the outer subcutaneous fat. 4. Plasma fatty acid, glucose and insulin concentrations were determined in fed and starved pigs. Starvation decreased the plasma insulin concentration and increased the non-esterified fatty acid concentration.

Adipose Tissue↗

Clearing-factor lipase in obese hyperglycaemic mice (ob-ob).

1. Clearing-factor lipase was assayed in acetone-ether-dried powders of heart and epididymal fat-pads of lean and genetically obese mice (ob/ob). In both tissues the enzyme activity in the adult was higher in the obese mice. 2. In heart the enzyme activity was unchanged from 8 to 48 weeks of age in lean mice, but in obese mice it increased between 8 and 12 weeks of age and remained elevated. 3. Starvation produced changes in the heart clearing-factor lipase activity in obese, but not lean, mice. 4. The clearing-factor lipase activity of epididymal fat-pads decreased rapidly during 24h starvation in both lean and obese mice, but the activity in the obese mice remained higher than that in lean mice. 5. Plasma triglyceride and cholesterol concentrations were determined in both lean and obese mice. Triglyceride concentrations were not greatly different, but the obese mice were hypercholesterolaemic. Plasma cholesterol concentrations were not correlated with changes in clearing-factor lipase activity.

Age Factors↗

Intestinal metabolism of fatty acids.

1. The effect of concentration on the oxidation and incorporation into lipids of lauric acid and linoleic acid by rings of rat small intestine has been studied in vitro. 2. In the absence of glucose, the oxidation of lauric acid in the range 0.01-5.0mm showed a maximum at 0.1mm. In the presence of glucose the maximum was at 0.5mm. The oxidation of linoleic acid in the presence of glucose increased throughout the concentration range 0.01-5.0mm. 3. The incorporation of lauric acid into lipids was maximal at 0.5-0.6mm in the presence of glucose, but at 10mm in the absence of glucose. At 0.8mm-lauric acid, in the presence of glucose, over 75% of the incorporated lauric acid was in triglycerides, but at 10mm they only contained 30%. The incorporation of glucose carbon into glycerides paralleled the incorporation of lauric acid. 4. In the range 0.01-2.5mm-linoleic acid the quantity incorporated into lipids increased. In the range 0.01-0.4mm linoleic acid was incorporated predominantly into triglycerides, but between 0.4 and 1.0mm most was in diglycerides, and between 2.5 and 5.0mm most was in monoglycerides. 5. The relationship of fatty acid concentration to the mechanism of absorption is discussed, together with the correlation between the distribution of the absorbed fatty acids within the tissue lipids and the lipase activity of intestinal mucosa.

Animals↗