The regulation of lipid synthesis in primary cultures of hepatocytes from nonketotic streptozotocin diabetic rats

Amatruda, John M.; Chang, Cecilia L.

doi:10.1016/0026-0495(83)90186-5

Cited by 19 publications

(10 citation statements)

References 17 publications

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“…Furthermore, it may not be insulin per se, but another factor that is induced by insulin in NIDDM patients that may be enhancing insulin sensitivity. Amatruda et al (58) have previously shown that in nonketotic streptozotocin diabetic rats administration of insulin improved insulin action in the liver. In contrast, in vitro insulin exposure of primary cultures of hepatocytes from these same diabetic insulin-resistant animals did not result in an improved insulin response (58).…”

Section: Discussionmentioning

confidence: 97%

“…Amatruda et al (58) have previously shown that in nonketotic streptozotocin diabetic rats administration of insulin improved insulin action in the liver. In contrast, in vitro insulin exposure of primary cultures of hepatocytes from these same diabetic insulin-resistant animals did not result in an improved insulin response (58). The factor(s) that regulate insulin action are largely unknown.…”

Section: Discussionmentioning

confidence: 97%

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Long-term effect of insulin on glucose transport and insulin binding in cultured adipocytes from normal and obese humans with and without non-insulin-dependent diabetes.

Sinha

Taylor²,

Pories³

et al. 1987

J. Clin. Invest.

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We have tested the hypothesis that in vitro exposure of insulin-resistant adipocytes with insulin results in improved insulin action. A primary culture system of adipocytes from obese subjects with or without non-insulin-dependent diabetes mellitus (NIDDM) and nonobese control subjects has been developed. The adipocytes when cultured in serum-free medium do not lose their original characteristics in regard to insulin binding and glucose transport. The adipocytes from three groups were incubated with insulin (0, 10-10 M, and lo-7 M) for 24 h at 370C, receptor-bound insuMin was dissociated, and basal and insulin (1 X 10-11_10-7 M)-stimulated glucose transport and "2I-insulin binding were determined. The 24-h insulin exposure of adipocytes from control subjects decreased basal and insulin-stimulated glucose transport. The effects of 1 X 1o-7 M insulin were more pronounced than 1 X 10-l' M insulin. Similarly, insulin exposure decreased insulin sensitivity and responsiveness of cultured adipocytes from obese and NIDDM patients. The insulin-induced reduction in insulin sensitivity and responsiveness for glucose transport in three groups were due to alterations at insulin binding and postbinding levels. In conclusion, insulin induces insulin resistance in control adipocytes and further worsens the insulin resistance of adipocytes from obese and NIDDM subjects. For insulin to improve the insulin resistance of adipocytes from NIDDM patients, either more prolonged in vitro insulin exposure and/or other hormonal factors might be required.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 97%

Long-term effect of insulin on glucose transport and insulin binding in cultured adipocytes from normal and obese humans with and without non-insulin-dependent diabetes.

Sinha

Taylor²,

Pories³

et al. 1987

J. Clin. Invest.

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“…Hepatocytes were prepared for primary culture in serum-free media (23) and placed onto 60-or 100-mm sterile petri dishes coated with rat tail collagen (100 gg/ml). The dishes were incubated for 4 h at 37°C in an atmosphere of 95% air/5% CO2, after which the medium and nonadherent cells were discarded and adherent cells were washed three times with 2.0 ml of 10 mM sodium phosphate, pH 7.4, 139 mM sodium chloride, and 0.1%, wt/vol, BSA.…”

Section: Methodsmentioning

confidence: 99%

“…Fresh media (2 ml/60-mm dish and 3 ml/100-mm dish) containing 0.2%, wt/vol, BSA was then added and cells were incubated overnight. At the conclusion of experiments and after the removal of media, cellular protein was determined (15,23 (25). Media lipoproteins were isolated by ultracentrifugation at salt densities of 1.063 g/ml and between 1.063 and 1.21 g/ml by the addition of solid sodium bromide as previously described (28).…”

Section: Methodsmentioning

confidence: 99%

Effects of nonketotic streptozotocin diabetes on apolipoprotein B synthesis and secretion by primary cultures of rat hepatocytes.

Sparks¹,

Sparks²,

Bolognino³

et al. 1988

J. Clin. Invest.

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The effects of hypoinsulinemic nonketotic streptozotocin diabetes on hepatic apo B synthesis and secretion was studied in primary cultures of rat hepatocytes. Diabetic rats were characterized by their significantly elevated serum glucose, apo B, and triglyceride levels, while serum insulin levels were less than a third of normal. Serum transaminase activities of diabetic rats were significantly elevated when compared with control rats, which was attributed to an increase in liver transaminase activity in diabetic rats. The pattern of enzyme activities of hepatocytes reflected that observed in livers of donor rats and the pattern was retained by primary cultures of hepatocytes over the culture period. Hepatocytes from diabetic rats secreted only one third of the apo B secreted by hepatocytes from control rats, which was determined by monoclonal immunoassay of rat total apo B. Decreases in secretion were confirmed by measurement of secretory [35S~methionine-labeled lipoprotein apo B radioactivity. The decreased apo B content of media of hepatocytes from diabetic rats was not due to increased apo B catabolism since hepatocytes from diabetic rats were shown to degrade less lipoprotein-apo B than hepatocytes from normal rats in control experiments. In addition, the apo B content of detergent-solubilized hepatocytes from diabetic rats was significantly less than that of hepatocytes from control rats. These results suggest that insulin is necessary for normal hepatic apo B synthesis and secretion and that the hyperlipidemia associated with hypoinsulinemia in vivo is primarily of intestinal origin.

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“…The increased rates of delivery of fatty acids to the liver makes this possible. (Although it has been found repeatedly that rates of VLDL-TAG secretion by isolated cultured hepatocytes and the perfused livers obtained from starved and diabetic rats have a much lower rate of secretion of TAG [90][91][92], these experiments may have underestimated the rates attainable, due to the inadequacy of the mixture of substrates provided to these preparations in itro, as demonstrated in [93]. )…”

Section: Acute Changes In Glycerolipid Partitioning During the Prandimentioning

confidence: 99%

Role of insulin in hepatic fatty acid partitioning: emerging concepts

Zammit

1996

Biochemical Journal

115

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The regulation of lipid synthesis in primary cultures of hepatocytes from nonketotic streptozotocin diabetic rats

Cited by 19 publications

References 17 publications

Long-term effect of insulin on glucose transport and insulin binding in cultured adipocytes from normal and obese humans with and without non-insulin-dependent diabetes.

Long-term effect of insulin on glucose transport and insulin binding in cultured adipocytes from normal and obese humans with and without non-insulin-dependent diabetes.

Effects of nonketotic streptozotocin diabetes on apolipoprotein B synthesis and secretion by primary cultures of rat hepatocytes.

Role of insulin in hepatic fatty acid partitioning: emerging concepts

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