The origin and glyceride distribution of fatty acids in rat adipose tissue.

Hollenberg, C. H.

doi:10.1172/jci105333

Cited by 42 publications

(27 citation statements)

References 27 publications

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“…Adipose tissue lipid content represents the result of a constant flux of new lipid accrual and ongoing lipolysis. As demonstrated previously (Hollenberg 1966), the increase in lipid content of rat adipose tissue was due to the accrual of predominantly unsaturated (plasma-derived) fatty acids, as opposed to saturated lipid from endogenous synthesis. Human adipose tissue also derives most of its lipid for storage from circulating triglycerides (Shrago et al 1969, Wilson et al 1973.…”

Section: Saquinavir Addedsupporting

confidence: 67%

“…To further examine the effect of HIV protease inhibitors on lipid metabolism, we studied the effects of two such drugs, saquinavir and indinavir, on LPL in vitro in 3T3-F442A adipocyte cultures. LPL-mediated triglyceride hydrolysis is one of the important factors in adipocyte lipid accumulation in humans and rats (Hollenberg 1966, Wilson et al 1973. The effects of these drugs on lipid accumulation and glucose transport were also investigated.…”

Section: Introductionmentioning

confidence: 99%

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The HIV protease inhibitor saquinavir impairs lipid metabolism and glucose transport in cultured adipocytes

Ranganathan

Kern²

2002

Journal of Endocrinology

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Treatment of HIV infection using protease inhibitors is frequently associated with lipodystrophy and impaired lipid and glucose metabolism. We examined the effect of saquinavir, one of the protease inhibitors, on lipid metabolism and glucose transport in cultured adipocytes. Saquinavir inhibited lipoprotein lipase (LPL) activity in 3T3-F442A and 3T3-L1 adipocytes. The inhibition of LPL was 81% at a concentration of 20 µg/ml. Another closely related drug, indinavir, had a small inhibitory effect. Saquinavir also inhibited the biosynthesis of lipids from [14 C]-acetate. Saquinavir increased the lipolysis.Saquinavir had no significant effect on the cellular protein synthesis or protein content. Saquinavir increased the basal glucose transport threefold and decreased insulinstimulated glucose transport by 35%. These studies suggest that some HIV protease inhibitors have direct effects on lipid and glucose metabolism. This inhibition of lipogenesis and glucose transport may explain some of the lipodystrophy, dyslipidemia and disturbed glucose metabolism with the clinical use of these drugs.

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Section: Saquinavir Addedsupporting

confidence: 67%

Section: Introductionmentioning

confidence: 99%

The HIV protease inhibitor saquinavir impairs lipid metabolism and glucose transport in cultured adipocytes

Ranganathan

Kern²

2002

Journal of Endocrinology

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“…In our two patients the experimental data were compatible with the existence of a highly active intra-adrenal compartment where plasma cholesterol is rapidly turned over as opposed to an adrenal reservoir where plasma cholesterol is stored and slowly renewed with a turnover time of several days; the contribution of these two compartments to the synthesis of the steroid hormones and the fractional turnover of the adrenal reservoir might vary from patient to patient and somewhat from day to day. According to this model the fate of plasma cholesterol in the adrenal cell might thus be quite analogous to that postulated for glycerophosphate and triglycerides in the adipose tissue (29,30). A fraction of plasma cholesterol entering the adrenal cell could be' rapidly catabolized in the cytoplasm and discharged as hydrocortisone, whereas plasma cholesterol *escaping immediate catabolism could be esterified (31) and stored in the lipid droplets.…”

Section: Discussionmentioning

confidence: 81%

Blood Cholesterol and Hydrocortisone Production in Man: Quantitative Aspects of the Utilization of Circulating Cholesterol by the Adrenals at Rest and under Adrenocorticotropin Stimulation*

Borkowski¹,

Levin²,

Delcroix³

et al. 1967

J. Clin. Invest.

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Summary. A kinetic study of the conversion of blood cholesterol into hydrocortisone was carried out in two patients through prolonged infusions of cholesterol-4-14C. The following points appear to be established by our observations:1) The infused tracer behaved metabolically like endogenous cholesterol; it could therefore serve as a means of labeling plasma cholesterol for investigating its utilization by the adrenal cortex.2) At rest, about 80% of hydrocortisone derived from plasma cholesterol, the other 20% thus being synthesized in situ from acetate and other unlabeled precursors.3) Under ACTH stimulation the participation of plasma cholesterol in the synthesis of hydrocortisone was the same as at rest; the conversion of plasma cholesterol into hydrocortisone was thus proportional to the production of glucocorticosteroids by the adrenal glands.4) The specific activities of hydrocortisone allowed us to trace its adrenal precursors including adrenal cholesterol. The kinetics of the replacement of adrenal cholesterol by plasma cholesterol underlined the functional heterogeneity of the former. The experimental data were compatible with the following model: A fraction of plasma cholesterol entering the adrenal cell is immediately available for metabolism and conversion into steroid hormones, and another fraction turns over slowly, representing some form of storage.

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“…In human adipose tissue, little of the lipid found in the storage droplet is synthesized de novo, but instead is derived from FFA of hydrolyzed triglycerides (2,21,22), therefore making LPL an important enzyme for lipid storage. In contrast, muscle uses FFA from circulating triglycerides for oxidation (3).…”

Section: Discussionmentioning

confidence: 99%

The regulation of adipose tissue and muscle lipoprotein lipase in runners by detraining.

Simsolo¹,

Ong²,

Kern³

1993

J. Clin. Invest.

101

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IntroductionTo study the mechanism of lipoprotein lipase (LPL) regulation by exercise, we recruited 16 healthy athletes to undergo a 2-wk period of detraining. Fasting fat and muscle biopsies were performed both before and after the detraining period. In muscle, detraining resulted in a decrease in LPL activity in both the heparin-releasable (HR) (-45%, P < 0.05) and cellular (ex- Triglyceride-derived FFA are taken up by tissues through the action oflipoprotein lipase (LPL)'(1), which is found predominantly in adipose tissue and muscle. In human adipose tissue, little FFA is synthesized from glucose, and therefore LPL is an important enzyme for lipid storage (2). In contrast, muscle uses FFA for oxidation (3). The LPL found in both adipose tissue and muscle contributes to the clearance of circulating triglyceride-rich lipoproteins.Previous studies have examined the effects of exercise on LPL activity, using a number of different exercise regimens (reviewed in reference 4). Studies of endurance training in human subjects showed significant increases in LPL activity, both in skeletal muscle and adipose tissue, as well as in postheparin plasma. Weight loss also yields increases in adipose LPL (5), however, and many studies of exercise did not control for weight loss during the exercise regimen. Kiens et al. (6) studied six healthy men in which LPL activity was measured in the knee extensors at rest and after 8 wk of training of one leg, while the other leg was not exercised and served as a control. They found a 70% increase in LPL activity in the trained leg compared with the nontrained one.A number of previous studies have examined the mechanism of LPL regulation, and have discovered that LPL may be regulated at multiple different cellular sites (7). This study was designed to examine the mechanism of regulation of LPL by exercise in adipose tissue and muscle. As described below, short-term changes in exercise altered LPL activity in both tissues through posttranslational changes. Methods Recruitment ofstudy subjects. 16 subjects (10 men and 6 women; age, 37±2 yr) were recruited for this study, and their characteristics are shown in Table I. All subjects were in good health, were taking no medications, and were running 2 32 km/wk, or performing an equivalent amount of aerobic exercise (one subject bicycled -600 km/ week). 6 of the 16 subjects ran a marathon within 1 mo preceding the study. To participate in the study, the subjects had to agree to detrain for 2 wk, and gave informed consent to the procedures. Detraining entailed no aerobic exercise, but just activities of daily living. Compliance with these instructions was judged to be excellent. This protocol was approved by the Internal Review Board of Cedars-Sinai Medical Center, and subjects gave informed consent to the procedures.

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The origin and glyceride distribution of fatty acids in rat adipose tissue.

Cited by 42 publications

References 27 publications

The HIV protease inhibitor saquinavir impairs lipid metabolism and glucose transport in cultured adipocytes

The HIV protease inhibitor saquinavir impairs lipid metabolism and glucose transport in cultured adipocytes

Blood Cholesterol and Hydrocortisone Production in Man: Quantitative Aspects of the Utilization of Circulating Cholesterol by the Adrenals at Rest and under Adrenocorticotropin Stimulation*

The regulation of adipose tissue and muscle lipoprotein lipase in runners by detraining.

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