The use of an automatic solids injection system for quantitative determination of plasma long chain non-esterified fatty acids by gas-liquid chromatography

Patterson

American Journal of Physiology-Endocrinology and Metabolism

2003

108

2 ). Stable isotope tracer techniques, in conjunction with compartmental modeling, were used to determine VLDL-triglyceride (TG) and apolipoprotein B-100 (apoB-100) secretion rates in lean women and in obese women before and after 10% weight loss. VLDL-TG and VLDL-apoB-100 secretion rates were similar in lean and obese women. Weight loss decreased the rate of VLDL-TG secretion by ϳ40% (from 0.41 Ϯ 0.05 to 0.23 Ϯ 0.03 mol ⅐ kg fat-free mass Ϫ1 ⅐ min Ϫ1 ; P Ͻ 0.05). The relative decline in VLDL-TG produced from nonsystemic fatty acids, derived from intraperitoneal and intrahepatic TG, was greater (61 Ϯ 7%) than the decline in VLDL-TG produced from systemic fatty acids, predominantly derived from subcutaneous TG (25 Ϯ 8%; P Ͻ 0.05). Weight loss did not affect VLDL-apoB-100 secretion rate. We conclude that weight loss decreases the rate of VLDL-TG secretion in women with abdominal obesity, primarily by decreasing the availability of nonsystemic fatty acids. There is a dissociation in the effect of weight loss on VLDL-TG and apoB-100 metabolic pathways that may affect VLDL particle size. lipoprotein; fatty acids; lipolysis OBESE PERSONS, particularly those with abdominal (upper-body) obesity, have an increased prevalence of dyslipidemia, manifested by increased fasting plasma triglyceride (TG) and decreased plasma HDL-cholesterol concentrations (12,26). These alterations in the plasma lipids are associated with an increased risk of coronary heart disease (2,8,9,12,26). The increase in plasma TG concentration is presumably related to increased hepatic secretion of VLDL, which is the major carrier of TG in plasma during postabsorptive conditions. VLDL-TG secretion is largely regulated by the availability of fatty acids derived from lipolysis of subcutaneous, intraperitoneal, and intrahepatic TG (4, 28, 41). Therefore, the increase in endogenous TG stores and lipolytic rates that is associated with obesity may be responsible for increased VLDL-TG secretion.Modest weight loss (5-10% of body wt) decreases plasma TG concentrations in obese persons (53). However, the mechanisms that are responsible for the alterations in plasma TG concentrations are not well understood. Moreover, results from several studies suggest that there may be sex differences in the response of lipoprotein kinetics to weight loss. We have recently found that both sex and obesity independently affect basal VLDL-TG metabolism (37). Studies conducted in hypertriglyceridemic (16) and obese (49) men found that weight loss decreased VLDL-TG (16) and VLDL-apolipoprotein B-100 (apoB-100) (16, 49) secretion rates. In contrast, a study conducted in obese women found that weight loss did not affect VLDL-TG secretion (20). However, the failure to show an effect of weight loss on VLDL-TG metabolism in obese women might have been confounded by negative energy balance and the methods used to assess VLDL kinetics, which did not account for tracer recycling or the conversion of tracer to other lipid components that can cause errors in calculating VLDL-TG secretion ra...

Section: Sample Analysesmentioning

confidence: 99%

Effect of weight loss on VLDL-triglyceride and apoB-100 kinetics in women with abdominal obesity

Patterson

American Journal of Physiology-Endocrinology and Metabolism

2003

108

“…Plasma glycerol concentration was determined by gas chromatography-mass spectrometry (GC-MS) after adding [2-13 C]glycerol to plasma as an internal standard. Plasma FFA concentrations were quantified by gas chromatography (model 5890-II; Hewlett-Packard, Palo Alto, CA) after adding heptadecanoic acid to plasma as an internal standard (36).…”

Section: Sample Analysesmentioning

confidence: 99%

Effect of gender on lipid kinetics during endurance exercise of moderate intensity in untrained subjects

Horowitz

American Journal of Physiology-Endocrinology and Metabolism

2002

125

100

. Effect of gender on lipid kinetics during endurance exercise of moderate intensity in untrained subjects. Am J Physiol Endocrinol Metab 283: E58-E65, 2002; 10.1152/ajpendo.00504.2001.-We evaluated lipid metabolism during 90 min of moderate-intensity (50% V O2 peak) cycle ergometer exercise in five men and five women who were matched on adiposity (24 Ϯ 2 and 25 Ϯ 1% body fat, respectively) and aerobic fitness (V O2 peak: 49 Ϯ 2 and 47 Ϯ 1 ml⅐ kg fat-free mass Ϫ1 ⅐ min Ϫ1 , respectively). Substrate oxidation and lipid kinetics were measured by using indirect calorimetry and [13 C]palmitate and [ 2 H5]glycerol tracer infusion. The total increase in glycerol and free fatty acid (FFA) rate of appearance (R a) in plasma during exercise (area under the curve above baseline) was ϳ65% greater in women than in men (glycerol Ra: 317 Ϯ 40 and 195 Ϯ 33 mol/kg, respectively; FFA R a: 652 Ϯ 46 and 453 Ϯ 70 mol/kg, respectively; both P Ͻ 0.05). Total fatty acid oxidation was similar in men and women, but the relative contribution of plasma FFA to total fatty acid oxidation was higher in women (76 Ϯ 5%) than in men (46 Ϯ 5%; P Ͻ 0.05). We conclude that lipolysis of adipose tissue triglycerides during moderate-intensity exercise is greater in women than in men, who are matched on adiposity and fitness. The increase in plasma fatty acid availability leads to a greater rate of plasma FFA tissue uptake and oxidation in women than in men. However, total fat oxidation is the same in both groups because of a reciprocal decrease in the oxidation rate of fatty acids derived from nonplasma sources, presumably intramuscular and possibly plasma triglycerides, in women.gender; fatty acids; lipolysis; exercise; stable isotopes ENDOGENOUS TRIGLYCERIDES are an important source of fuel for working muscles during endurance exercise (24). Increased lipolysis of adipose tissue triglycerides during exercise, which is mediated primarily by an increase in ␤-adrenergic receptor stimulation (1, 20), releases fatty acids into the systemic circulation for delivery to skeletal muscle for oxidation. In addition, exercise stimulates lipolysis of intramuscular triglycerides, which release fatty acids that are directly oxidized by local mitochondria.The effect of gender on the mobilization and oxidation of endogenous triglycerides during exercise is unclear because of conflicting results from different studies. Most studies that evaluated regional and whole body lipolytic rates during moderate-intensity endurance exercise, by using either microdialysis probes or isotope tracers, have reported that lipolytic rates in women are greater than in men (1,6,14,23). Others, however, found that the lipolytic response to exercise is the same in men and women (5). Similarly, studies that evaluated substrate oxidation during exercise have reported that women use more fat and less carbohydrate than men (3,6,15,26,49), whereas other studies found that relative fuel use was similar in men and women (5,8,14,30,41). The reason(s) for the discrepancies between studies is not...

“…Total plasma TG and VLDL-TG concentrations were measured using a spectrophotometric enzymatic kit (Sigma Chemicals, St. Louis, MO). Plasma fatty acid concentrations were quantified by gas chromatography (model 5890-II; Hewlett-Packard, Palo Alto, CA) after heptadecanoic acid was added to plasma as an internal standard (30).…”

Section: Sample Analysesmentioning

confidence: 99%

VLDL-triglyceride kinetics during hyperglycemia-hyperinsulinemia: effects of sex and obesity

Patterson

American Journal of Physiology-Endocrinology and Metabolism

et al. 2003

. VLDL-triglyceride kinetics during hyperglycemia-hyperinsulinemia: effects of sex and obesity. Am J Physiol Endocrinol Metab 284: E708-E715, 2003. First published December 10, 2002 10.1152/ajpendo. 00411.2002We have previously shown that sex and obesity independently affect basal very low density lipoprotein (VLDL)-triglyceride (TG) kinetics. In the present study, we investigated the effect of hyperglycemia-hyperinsulinemia on VLDL-TG kinetics in lean and obese men and women (n ϭ 6 in each group). VLDL-TG kinetics were measured during basal, postabsorptive conditions and during glucose infusion (5.5 mg ⅐ kg FFM Ϫ1 ⅐ min Ϫ1 ) by using [ 2 H5]glycerol bolus injection in conjunction with compartmental modeling analysis. Basal VLDL-TG secretion in plasma was greater in obese than in lean men (7.8 Ϯ 0.6 and 2.9 Ϯ 0.4 mol ⅐ l plasma Ϫ1 ⅐ min Ϫ1 ; P Ͻ 0.001) but was not different in lean and obese women (5.0 Ϯ 1.1 and 5.9 Ϯ 1.1 mol ⅐ l plasma Ϫ1 ⅐ min Ϫ1 ). Glucose infusion decreased the VLDL-TG secretion rate by ϳ50% in lean and obese men and in lean women (to 1.5 Ϯ 0.4, 4.0 Ϯ 0.6, and 2.2 Ϯ 0.4 mol ⅐ l plasma Ϫ1 ⅐ min Ϫ1 , respectively; all P Ͻ 0.05) but had no effect on the VLDL-TG secretion rate in obese women (4.9 Ϯ 1.0 mol ⅐ l plasma Ϫ1 ⅐ min Ϫ1 ). These results demonstrate that both sex and adiposity affect the regulation of VLDL-TG metabolism. Glucose and insulin decrease VLDL-TG production in both lean men and lean women; obesity is associated with resistance to the glucoseand insulin-mediated suppression of VLDL-TG secretion in women, but not in men.hyperglycemia; coronary heart disease; hypertriglyceridemia ALTERATIONS IN VERY LOW DENSITY lipoprotein (VLDL)-triglyceride (TG) metabolism are involved in the pathogenesis of coronary heart disease (CHD). Epidemiological studies have demonstrated a direct relationship between plasma TG concentration and the risk of CHD in both men and women (7, 10). In addition, an increase in plasma VLDL-TG concentration is associated with a decrease in plasma high density lipoproteincholesterol (10, 24) and an increase of low density lipoprotein particles (2, 10), which are also important risk factors for CHD (2, 6, 10).Hepatic fatty acid availability is a major regulator of VLDL-TG production. In lean subjects, the majority (Ͼ75%) of fatty acids in VLDL-TG are derived from plasma (3,34,37), and increasing the delivery of plasma free fatty acids (FFA) to the liver stimulates the secretion of VLDL-TG in plasma (25). Glucose and insulin are also involved in the regulation of VLDL-TG secretion in plasma because of their effects on fatty acid metabolism. In lean subjects, both insulin (26-28) and glucose (1) acutely decrease VLDL-TG secretion predominantly by their suppressive effects on whole body lipolysis and plasma FFA availability. However, when the insulin-induced decrease in plasma FFA concentration is prevented by infusing Intralipid and heparin, insulin (i.e., hyperinsulinemic euglycemic clamp) suppresses VLDL-TG production (27), whereas glucose (with the concomitant in...