Glucose Metabolism and Response to Insulin of Isolated Fat Cells and Epididymal Fat Pads

Gliemann, Jørgen

doi:10.1111/j.1365-201x.1968.tb10857.x

Cited by 7 publications

(7 citation statements)

References 12 publications

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“…From the present results, it seems likely that the inhibition of glucose metabolism in isolated adipocytes is the result of a specific action on the translocation of the sugar across the plasma membrane, for the following reasons. Since glucose metabolism to CO2 and lipids constitutes greater than 80% of total glucose metabolism in isolated fat-cells (Gliemann, 1968), and since it has been previously shown that glucose transport is the rate-limiting step in its subsequent metabolism (Crofford, 1967;Crofford & Renold, 1965), the observed inhibition is most likely to be due to inhibition at this site. Further evidence is provided by experiments in which it was found that uptake of 2-deoxyglucose was also decreased by cytochalasin B.…”

Section: Discussionmentioning

confidence: 97%

Effects of cytochalasin B, colchicine and vincristine on the metabolism of isolated fat-cells

Loten¹,

Jeanrenaud²

1974

Biochemical Journal

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1. Colchicine and vincristine only slightly inhibit the metabolism of glucose to CO(2) and lipids by isolated fat-cells. 2. Prolonged incubation with these agents causes no further inhibition. 3. Cytochalasin B, however, inhibits glucose metabolism to both CO(2) and lipids in fat-cells. 4. However, at a concentration that causes a strong inhibition of glucose metabolism cytochalasin B is without effect on the metabolism of pyruvate, lactate or arginine to these end products. The uptake of labelled alpha-aminoisobutyrate is likewise not modified. Similarly it does not affect release of glycerol or free fatty acid, or the actions of adrenaline, insulin or caffeine on these parameters. At 10mug/ml it slightly lowers ATP concentrations, an effect that does not occur at 2mug/ml. 5. The transport of fructose into adipocytes by a specific fructose-transport system is also not affected by the agent, but the uptake of 2-deoxyglucose is strongly inhibited. It is concluded that cytochalasin B may specifically inhibit the glucose-transport system of isolated fat-cells. 6. Cytochalasin A has a much weaker action than cytochalasin B on glucose metabolism.

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Section: Discussionmentioning

confidence: 97%

Effects of cytochalasin B, colchicine and vincristine on the metabolism of isolated fat-cells

Loten¹,

Jeanrenaud²

1974

Biochemical Journal

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“…The rate of conversion of tracer glucose (0.7 ~tmol/1) was proportional to methylglucose transport under all conditions, indicating that transport was rate determining for the metabolism of glucose at this very low concentration. This comparison has not been carried out before but it has been noted by others that transport of glucose in high concentrations is not rate limiting in small or large cells in the presence of insulin [7,20], and that metabolism becomes rate limiting at lower glucose concentrations in larger cells [4,23]. The very small effect of insulin in large cells on the rate of conversion of glucose at physiological concentrations is therefore to a considerable extent caused by their low capacity to metabolise glucose [7,[20][21][22][23].…”

Section: Transport and Metabolandmmentioning

confidence: 99%

“…The total volume was 0.5 ml. It has previously been shown that bacitracin markedly inhibits extracellular insulin degradation without interfering with receptor-mediated degradation of insulin or its effect on hexose transport [20,12]. The cells were incubated for 45 min at 37 ~ The incubation was terminated and the cells recovered as described previously [10].…”

Section: Insulin Bindingmentioning

confidence: 99%

“…3) over the entire cell size range. The rate of conversion of glucose to CO2 and lipids, which accounts for about 80% of the rate of glucose uptake [7,20] was about half of the methylglucose transport rate. The data show that the rate of conversion of tracer glucose is a reasonable reflection of the changes in methylglucose transport as a function of cell size, whereas the rate of uptake of deoxyglucose is not.…”

Section: Hexose Transportmentioning

confidence: 99%

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Insulin binding and hexose transport in rat adipocytes

et al. 1980

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Insulin binding, initial velocity of [14C]methylglucose transport, uptake of [14C]deoxyglucose and conversion of [U-14C]glucose to CO2, glyceride-glycerol and fatty acids were measured at 37 degrees C in adipocytes from rats of different weights (135-450 g) and therefore with different mean cell volumes (53-389 pl). Insulin binding per cell increased with increasing cell size and binding was 2.3 times higher in the largest cells than in the smallest cells with tracer alone. The difference was largely accounted for by an increase in the apparent affinity. Influx of methylglucose per cell increased with increasing cell size in the absence of insulin and remained constant as a function of cell size in its presence. The effect of insulin ranged from 11 fold in small cells to 3.5 fold in large cells. The rat of conversion of [U-14C]glucose to CO2 and lipids was about half of the rate of methylglucose transport under all conditions. In contrast, the uptake of deoxyglucose in insulin-stimulated cells decreased markedly with increasing cell size. Increasing cell size caused a small decrease in sensitivity which could be explained by a smaller amont of insulin bound per unit surface area. The results show that increasing cell size/animal weight causes changes in insulin binding which may explain changes in sensitivity. In addition, the hexose transport system is modified in a way which is not explained by changes in insulin binding. Finally, changes in deoxyglucose uptake with cell size do not parallel changes in methylglucose transport.

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“…Interestingly, at a constant insulin concentration, low concentrations of glucose were preferentially metabolized to glycogen (36), and glucose conversion to glycogen by the adipocyte was more sensitive to insulin than either CO 2 production or triglyceride synthesis (43). These experiments led to the hypothesis that glucose entering the fat cell is first used to replenish glycogen stores, but this pathway is saturated quickly and glucose is subsequently shunted to triglyceride synthesis and ATP production (21,43).…”

mentioning

confidence: 99%

Transgenic overexpression of protein targeting to glycogen markedly increases adipocytic glycogen storage in mice

Jurczak

Danos²,

Rehrmann³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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-Adipocytes express the rate-limiting enzymes required for glycogen metabolism and increase glycogen synthesis in response to insulin. However, the physiological function of adipocytic glycogen in vivo is unclear, due in part to the low absolute levels and the apparent biophysical constraints of adipocyte morphology on glycogen accumulation. To further study the regulation of glycogen metabolism in adipose tissue, transgenic mice were generated that overexpressed the protein phosphatase-1 (PP1) glycogen-targeting subunit (PTG) driven by the adipocyte fatty acid binding protein (aP2) promoter. Exogenous PTG was detected in gonadal, perirenal, and brown fat depots, but it was not detected in any other tissue examined. PTG overexpression resulted in a modest redistribution of PP1 to glycogen particles, corresponding to a threefold increase in the glycogen synthase activity ratio. Glycogen synthase protein levels were also increased twofold, resulting in a combined greater than sixfold enhancement of basal glycogen synthase specific activity. Adipocytic glycogen levels were increased 200-to 400-fold in transgenic animals, and this increase was maintained to 1 yr of age. In contrast, lipid metabolism in transgenic adipose tissue was not significantly altered, as assessed by lipogenic rates, weight gain on normal or high-fat diets, or circulating free fatty acid levels after a fast. However, circulating and adipocytic leptin levels were doubled in transgenic animals, whereas adiponectin expression was unchanged. Cumulatively, these data indicate that murine adipocytes are capable of storing far higher levels of glycogen than previously reported. Furthermore, these results were obtained by overexpression of an endogenous adipocytic protein, suggesting that mechanisms may exist in vivo to maintain adipocytic glycogen storage at a physiological set point.insulin; glycogen synthesis; lipogenesis; protein phosphatase-1; targeting subunit CIRCULATING ENERGY SOURCES are maintained in a narrow homeostatic range across a wide variety of physiological conditions through the coordinate regulation of energy uptake, consumption, storage, and release by the principal metabolic tissues, namely adipose tissue, liver, and skeletal muscle. During times of energy deficit, adipose tissue is a primary site for energy provision via the hydrolysis of stored triglyceride to release free fatty acid (FFA) for ATP production and glycerol for hepatic gluconeogenesis. Conversely, following a meal, dietary lipid is stored by adipose tissue, and glucose is disposed of as glycogen by the skeletal muscle and to a lesser extent by the liver. Alternately, glucose can be utilized postprandially by the liver and adipocytes for de novo lipogenesis and long-term storage as triglyceride. However, adipocytes also store glucose as glycogen, albeit at substantially lower rates than in skeletal muscle and liver, so the physiological role of adipocytic glycogen metabolism remains unclear.In addition to its role in lipid metabolism, adipose tissue functions as an...

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Glucose Metabolism and Response to Insulin of Isolated Fat Cells and Epididymal Fat Pads

Cited by 7 publications

References 12 publications

Effects of cytochalasin B, colchicine and vincristine on the metabolism of isolated fat-cells

Effects of cytochalasin B, colchicine and vincristine on the metabolism of isolated fat-cells

Insulin binding and hexose transport in rat adipocytes

Transgenic overexpression of protein targeting to glycogen markedly increases adipocytic glycogen storage in mice

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