Fatty acid uptake and esterification in adipose tissue

Shapiro, B.; Chowers, I.; Rose, G.

doi:10.1016/0006-3002(57)90292-5

Cited by 210 publications

(26 citation statements)

References 3 publications

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“…Exogenous 14C-labeled fatty acids can be both oxidized (14) and esterified (1,33,34) by adipose tissue in vitro. They can be used to label the pool of intracellular fatty acids permitting the measurement of changes in oxidation and esterification rate (14).…”

Section: Discussionmentioning

confidence: 99%

Carnitine and Development of Newborn Adipose Tissue

et al. 1978

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Section: Discussionmentioning

confidence: 99%

Carnitine and Development of Newborn Adipose Tissue

et al. 1978

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“…Furthermore, it is assumed that very low-density lipoproteins account for a negligible proportion of glycerol flux, as has been observed in rats (42), and that mesenteric lipolysis is minimal, as observed in dogs and humans in the resting state (3,5,39). Significant glycerol metabolism is not possible within adipocytes since glycerol kinase, the enzyme necessary for the formation of glycerol into a triglyceride backbone (i.e., ␣-glycerophosphate), does not exist within the adipocytes where free fatty acid (FFA) oxidation occurs (35,37). Thus, for every glycerol produced through lipolysis, three FFA molecules are presumed to be released.…”

Section: Sample Processingmentioning

confidence: 97%

Lipolysis and glycerol gluconeogenesis in simultaneously fasting and lactating northern elephant seals

Houser¹,

Champagne²,

Crocker³

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Adult female elephant seals (Mirounga angustirostris) combine long-term fasting with lactation and molting. Glycerol gluconeogenesis has been hypothesized as potentially meeting all of the glucose requirements of the seals during these fasts. To test this hypothesis, a primed constant infusion of [2-14 C]glycerol was administered to 10 ten adult female elephant seals at 5 and 21-22 days postpartum and to 10 additional adult females immediately after the molt. Glycerol kinetics, rates of lipolysis, and the contribution of glycerol to glucose production were determined for each period. Plasma metabolite levels as well as insulin, glucagon, and cortisol were also measured. Glycerol rate of appearance was not significantly correlated with mass (P ϭ 0.14, r 2 ϭ 0.33) but was significantly related to the percentage of glucose derived from glycerol (P Ͻ 0.01, r 2 ϭ 0.81) during late lactation. The contribution of glycerol to glucose production was Ͻ3% during each fasting period, suggesting a lower contribution to gluconeogenesis than is observed in other long-term fasting mammals. Because of a high rate of endogenous glucose production in fasting elephant seals, it is likely that glycerol gluconeogenesis still makes a substantial contribution to the substrate needs of glucose-dependent tissues. The lack of a relationship between glucoregulatory hormones and glycerol kinetics, glycerol gluconeogenesis, and metabolites supports the proposition that fasting elephant seals do not conform to the traditional insulinglucagon model of substrate metabolism. reesterification; lipid metabolism; lactogenesis; glucagon; insulin GLUCONEOGENESIS IS an important physiological process in maintaining blood glucose levels during fasting and can meet Ͼ90% of glucose needs after just 2 days of fasting (28). Both amino acids and glycerol can be metabolized to glucose when exogenous carbohydrate becomes unavailable. However, under long-term fasting conditions the loss of protein is generally minimized to stay the eventual loss of organ function that results from protein depletion. Under these conditions glycerol becomes an increasingly important gluconeogenic precursor. In the postabsorptive state, the conversion of glycerol to glucose accounts for ϳ3-4.5% of glucose production; however, after fasting for several days, the contribution of glycerol to glucose production increases to ϳ10 -22% (2, 7, 29). After weeks of fasting glycerol can contribute up to 60% of glucose production (7), although the basis for this calculation has come into question because of methodological issues related to the separation of radiolabeled glycerol from radiolabeled glucose (2). Thus, during long-duration fasts, the availability of lipid stores not only serves to provide energy via fatty acid oxidation but also contributes to meeting the energetic costs of glucose-dependent tissues.Northern elephant seals (Mirounga angustirostris) undertake prolonged fasts of 1-3 mo. Adult females undertake two fasts each year, one while lactating and another while molting. Bot...

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“…The cellular release of glycerol, which cannot be directly esterified by adipocytes (45,46), provides an estimate of HSL activity. In contrast, the NEFA liberated by HSL can be either released into the medium or re-esterified, so that differences in the amount of NEFA released and the amount expected on the basis of glycerol release reflect the effects of NEFA re-esterification.…”

Section: H Ruan and Hj Pownallmentioning

confidence: 99%

Overexpression of 1-Acyl-Glycerol-3-Phosphate Acyltransferase-αEnhances Lipid Storage in Cellular Models of Adipose Tissue and Skeletal Muscle

Ruan

Pownall

2001

Diabetes

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Plasma nonesterified fatty acids (NEFA) at elevated concentrations antagonize insulin action and thus may play a critical role in the development of insulin resistance in type 2 diabetes. Plasma NEFA and glucose concentrations are regulated, in part, by their uptake into peripheral tissues. Cellular energy uptake can be increased by enhancing either energy transport or metabolism. The effects of overexpression of 1-acylglycerol-3-phosphate acyltransferase (AGAT)-␣, which catalyzes the second step in triglyceride formation from glycerol-3-phosphate, was studied in 3T3-L1 adipocytes and C2C12 myotubes. In myotubes, overexpression of AGAT-␣ did not affect total [ T ype 2 diabetes is characterized, in part, by excess energy as glucose and nonesterified fatty acids (NEFA) within the plasma compartment. Moreover, an elevated plasma NEFA concentration has been increasingly recognized as a systemic mediator of insulin resistance in type 2 diabetes (1-5). Excess plasma NEFA can inhibit insulin-stimulated glucose utilization in muscle (1-4) and promote hepatic production of glucose (4-6) and VLDL triglyceride (TG) (7,8). Acute systemic administration of NEFA inhibits glucose disposal in muscle in a dose-dependent fashion (4) and increases hepatic glucose output (5,6). Reduction of plasma NEFA concentration improves glucose utilization (9-11), enhances the suppression of hepatic glucose production by insulin (12), and reduces hyperinsulinemia in patients with type 2 diabetes (13). Thus, plasma NEFA elevation may be mechanistically linked to the cluster of metabolic abnormalities seen in type 2 diabetes, including hyperglycemia, hyperinsulinemia, and dyslipidemia.Skeletal muscle and adipose tissue are major sites of energy utilization. Most of the glucose and NEFA taken up by resting muscle is converted to glycogen (14) and TG (15). Because of its mass, skeletal muscle is a significant storage site for excess plasma NEFA in patients with type 2 diabetes (16) and in animal models of the disease (17,18). However, the accumulation of intramuscular TG may increase lipid oxidation and decrease glucose uptake and insulin sensitivity (18,19). In contrast, increasing NEFA and glucose uptake in adipose tissue could reduce systemic NEFA availability and would eventually improve insulin sensitivity in liver and muscle.Energy uptake can be increased by enhancing either of the proposed rate-limiting steps of energy utilization, i.e., energy transport across the plasma membrane or energy metabolism within the cell. Indeed, an increase in glucose transport (20)(21)(22) or metabolism (23,24) promotes glucose utilization in cultured cells and transgenic animals. Moreover, glucose metabolism appears to be rate limiting under conditions of enhanced glucose transport (22,(25)(26)(27)(28)(29). Less is known about the regulation of NEFA uptake. Overexpression of long-chain fatty acid transport protein (FATP) increases NEFA uptake in 3T3-L1 fibroblasts (30). On the other hand, an increase in cytoplasmic fatty acyl-CoA synthase (FACS) activity wit...

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Fatty acid uptake and esterification in adipose tissue

Cited by 210 publications

References 3 publications

Carnitine and Development of Newborn Adipose Tissue

Carnitine and Development of Newborn Adipose Tissue

Lipolysis and glycerol gluconeogenesis in simultaneously fasting and lactating northern elephant seals

Overexpression of 1-Acyl-Glycerol-3-Phosphate Acyltransferase-αEnhances Lipid Storage in Cellular Models of Adipose Tissue and Skeletal Muscle

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