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Biomedical subjects

Bettina Mittendorfer

Publications and source records attributed to Bettina Mittendorfer.

At least 19 recordsLinked to original sources
PubMed2006

Blunted lipolysis and fatty acid oxidation during moderate exercise in HIV-infected subjects taking HAART.

The protease inhibitor (PI) ritonavir (RTV) has been associated with elevated resting lipolytic rate, hyperlipidemia, and insulin resistance/glucose intolerance. The purpose of this study was to examine relationships between lipolysis and fatty acid (FA) oxidation during rest, moderate exercise and recovery, and measures of insulin sensitivity/glucose tolerance and fat redistribution in HIV-positive subjects taking RTV (n=12), HAART but no PI (n=10), and HIV-seronegative controls (n=10). Stable isotope tracers [1-(13)C]palmitate and [1,1,2,3,3-(2)H5]glycerol were continuously infused with blood and breath collection during 1-h rest, 70-min submaximal exercise (50% VO2 peak), and 1-h recovery. Body composition was evaluated using DEXA, MRI, and MRS, and 2-h oral glucose tolerance tests with insulin monitoring were used to evaluate glucose tolerance and insulin resistance. Lipolytic and FA oxidation rates were similar during rest and recovery in all groups; however, they were lower during moderate exercise in both HIV-infected groups [glycerol Ra: HIV+RTV 5.1+/-1.2 vs. HIV+no PI 5.9+/-2.8 vs. Control 7.4+/-2.2 micromol.kg fat-free mass (FFM)-1.min-1; palmitate oxidation: HIV+RTV 1.6+/-0.8 vs. HIV+no PI 1.6+/-0.8 vs. Control 2.5+/-1.7 micromol.kg FFM.min, P<0.01]. Fasting and orally-challenged glucose and insulin values were similar among groups. Lipolytic and FA oxidation rates were blunted during moderate exercise in HIV-positive subjects taking HAART. Lower FA oxidation during exercise was primarily due to impaired plasma FA oxidation, with a minor contribution from lower nonplasma FA oxidation. Regional differences in adipose tissue lipolysis during rest and moderate exercise may be important in HIV and warrant further study.

Adult↗
PubMed2006

No effect of menstrual cycle phase on basal very-low-density lipoprotein triglyceride and apolipoprotein B-100 kinetics.

Dyslipidemia, manifested by increased plasma triglyceride (TG), increased total and LDL-cholesterol concentrations and decreased HDL-cholesterol concentration, is an important risk factor for cardiovascular disease. Premenopausal women have a less atherogenic plasma lipid profile and a lower risk of cardiovascular disease than men, but this female advantage disappears after menopause. This suggests that female sex steroids affect lipoprotein metabolism. The impact of variations in the availability of ovarian hormones during the menstrual cycle on lipoprotein metabolism is not known. We therefore investigated whether very-low-density lipoprotein (VLDL)-TG and VLDL-apolipoprotein B-100 (apoB-100) kinetics are different during the follicular (FP) and luteal phases (LP) of the menstrual cycle. We studied seven healthy, premenopausal women (age 27 +/- 2 yr, BMI 25 +/- 2 kg/m(2)) once during FP and once during LP. We measured VLDL-TG, VLDL-apoB-100, and plasma free fatty acid (FFA) kinetics by using stable isotope-labeled tracers, VLDL subclass profile by nuclear magnetic resonance spectroscopy, whole body fat oxidation by indirect calorimetry, and the plasma concentrations of lipoprotein lipase (LPL) and hepatic lipase (HL) by ELISA. VLDL-TG and VLDL-apoB-100 concentrations in plasma, VLDL-TG and VLDL-apoB-100 secretion rates and mean residence times, VLDL subclass distribution, FFA concentration and rate of appearance in plasma, whole body substrate oxidation, and LPL and HL concentrations in plasma were not different during the FP and the LP. We conclude that VLDL-TG and VLDL-apoB-100 metabolism is not affected by menstrual cycle phase.

Adult↗
PubMed2006

Insulin resistance of muscle protein metabolism in aging.

A reduced response of older skeletal muscle to anabolic stimuli may contribute to the development of sarcopenia. We hypothesized that muscle proteins are resistant to the anabolic action of insulin in the elderly. We examined the effects of hyperinsulinemia on muscle protein metabolism in young (25+/-2 year) and older (68+/-1 year) healthy subjects using stable isotope tracer techniques. Leg blood flow was higher in the young at baseline and increased during hyperinsulinemia, whereas it did not change in the elderly. Glucose concentrations and muscle uptake were not different between groups at baseline and during hyperinsulinemia. Leg phenylalanine net balance was not different at baseline and significantly increased in both groups with hyperinsulinemia (P<0.05) but to a greater extent in the young (P<0.05). Muscle protein synthesis increased only in the young during hyperinsulinemia. Muscle protein breakdown did not significantly change in either group, although it tended to decrease in the elderly. Changes in muscle protein synthesis were correlated with changes in leg amino acid delivery (R=0.89; P=0.0001) and blood flow (R=0.90; P<0.0001). In conclusion, skeletal muscle protein synthesis is resistant to the anabolic action of insulin in older subjects, which may be an important contributor to the development of sarcopenia.

Adult↗
PubMed2006

Influence of TNF-alpha and IL-6 infusions on insulin sensitivity and expression of IL-18 in humans.

Inflammation is associated with insulin resistance, and both tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 may affect glucose uptake. TNF induces insulin resistance, whereas the role of IL-6 is controversial. High plasma levels of IL-18 are associated with insulin resistance in epidemiological studies. We investigated the effects of TNF and IL-6 on IL-18 gene expression in skeletal muscle and adipose tissue. Nine human volunteers underwent three consecutive interventions, receiving an infusion of recombinant human (rh)IL-6, rhTNF, and saline. Insulin sensitivity was assessed by measurement of whole body glucose uptake with the stable isotope tracer method during a euglycemic hyperinsulinemic clamp (20 mU.min(-1).kg(-1)), which was initiated 1 h after the IL-6-TNF-saline infusion. Cytokine responses were measured in plasma, muscle, and fat biopsies. Plasma concentrations of TNF and IL-6 increased 10- and 38-fold, respectively, during the cytokine infusions. Whole body insulin-mediated glucose uptake was significantly reduced during TNF infusion but remained unchanged during IL-6 infusion. TNF induced IL-18 gene expression in muscle tissue, but not in adipose tissue, whereas IL-6 infusion had no effect on IL-18 gene expression in either tissue. We conclude that TNF-induced insulin resistance of whole body glucose uptake is associated with increased IL-18 gene expression in muscle tissue, indicating that TNF and IL-18 interact, and both may have important regulatory roles in the pathogenesis of insulin resistance.

Adipose Tissue↗
PubMed2006

Gastric bypass surgery improves metabolic and hepatic abnormalities associated with nonalcoholic fatty liver disease.

BACKGROUND & AIMS: Most patients with extreme obesity have nonalcoholic fatty liver disease (NAFLD). Although gastric bypass (GBP) surgery is the most common bariatric operation performed in obese patients in the United States, the effect of GBP surgery-induced weight loss on the metabolic and hepatic abnormalities associated with NAFLD are not clear. METHODS: Whole-body glucose, fatty acid and lipoprotein kinetics, liver histology, and hepatic cellular factors involved in inflammation and fibrogenesis were evaluated in 7 extremely obese subjects (body mass index, 58 +/- 4 kg/m(2)) before and 1 year after GBP surgery. RESULTS: At 1 year after surgery, subjects lost 29% +/- 5% of initial body weight (P < .01); palmitate rate of appearance in plasma, an index of adipose tissue lipolysis, decreased by 47% +/- 4% (P < .01); endogenous glucose production rate decreased by 27% +/- 7% (P < .01); and very-low-density lipoprotein-triglyceride secretion rate decreased by 44% +/- 9% (P < .05). In addition, GBP surgery-induced weight loss decreased hepatic steatosis but did not change standard histologic assessments of inflammation and fibrosis. However, there was a marked decrease in hepatic factors involved in regulating fibrogenesis (collagen-alpha1(I), transforming growth factor-beta1, alpha-smooth muscle actin, and tissue inhibitor of metalloproteinase 1 expression and alpha-smooth muscle actin content) and inflammation (macrophage chemoattractant protein 1 and interleukin 8 expression) (P < .05, compared with values before weight loss). CONCLUSIONS: These data demonstrate that weight loss induced by GBP surgery normalizes the metabolic abnormalities involved in the pathogenesis and pathophysiology of NAFLD and decreases the hepatic expression of factors involved in the progression of liver inflammation and fibrosis.

Analysis of Variance↗
PubMed2005

Lipid metabolism response to a single, prolonged bout of endurance exercise in healthy young men.

To discover the alterations in lipid metabolism linked to postexercise hypotriglyceridemia, we measured lipid kinetics, lipoprotein subclass distribution and lipid transfer enzymes in seven healthy, lean, young men the day after 2 h of cycling and rest. Compared with rest, exercise increased fatty acid rate of appearance and whole body fatty acid oxidation by approximately 65 and 40%, respectively (P < 0.05); exercise had no effect on VLDL-triglyceride (TG) secretion rate, increased VLDL-TG plasma clearance rate by 40 +/- 8%, and reduced VLDL-TG mean residence time by approximately 40 min and VLDL-apolipoprotein B-100 (apoB-100) secretion rate by 24 +/- 8% (all P < 0.05). Exercise also reduced the number of VLDL but almost doubled the number of IDL particles in plasma (P < 0.05). Muscle lipoprotein lipase content was not different after exercise and rest, but plasma lipoprotein lipase concentration increased by approximately 20% after exercise (P < 0.05). Plasma hepatic lipase and lecithin:cholesterol acyltransferase concentrations were not affected by exercise, whereas cholesterol ester transfer protein concentration was approximately 10% lower after exercise than after rest (P = 0.052). We conclude that 1) greater fatty acid availability after exercise does not stimulate VLDL-TG secretion, probably because of the increase in fatty acid oxidation and possibly also fatty acid use for restoration of tissue TG stores; 2) reduced secretion of VLDL-apoB-100 lowers plasma VLDL particle concentration; and 3) increased VLDL-TG plasma clearance maintains low plasma TG concentration but is not accompanied by similar increases in subsequent steps of the delipidation cascade. Acutely, therefore, the cardioprotective lowering of plasma TG and VLDL concentrations by exercise is counteracted by a proatherogenic increase in IDL concentration.

Adult↗
PubMed2005

Sexual dimorphism in human lipid metabolism.

The existing work demonstrates that striking differences exist between men and women in lipid kinetics. These differences cannot be explained simply by the presence and action of sex hormones and are not always due to secondary, phenotypic traits that characterize men and women (e.g., body-composition, regional fat distribution). In fact, some of these secondary traits may even be the result of sexual dimorphism in metabolism, and being of female or male genotype also determines intermediary metabolism. This review provides an overview of the currently available information regarding sexual dimorphism in human lipid metabolism but does not provide an in-depth account of current knowledge (due to limited space); it will be a broad introduction to those interested in the field and will, hopefully, stimulate further efforts to unravel the secrets of male and female metabolism. What has been discovered so far regarding differences in lipid metabolism between men and women is likely only the tip of the iceberg; clearly, more work is necessary to fully understand human substrate metabolism and the implications the presence of sexual dimorphism in the control of substrate kinetics has on the prevention and treatment of disease.

Female↗
PubMed2005

Insulin resistance: sex matters.

PURPOSE OF REVIEW: This review summarizes recent advances in our understanding of the differences between the sexes in relation to insulin resistance. Alterations in the body's sensitivity to insulin cause a series of metabolic abnormalities representing essentially the metabolic syndrome (i.e. high fasting plasma triglyceride and glucose and low HDL-cholesterol concentrations, hypertension, abdominal obesity) and type 2 diabetes. Although our knowledge of the causes and consequences of impairments in the insulin signaling pathway at the metabolic, cellular and molecular level has progressed rapidly and continues to do so, serious attempts to discover whether and how sex affects the metabolic control by insulin has only recently started to evolve. RECENT FINDINGS: The most significant recent findings include data that suggest that females are intrinsically more insulin resistant than males, possibly because of specific sex-linked gene expression and the resulting differences in metabolic control elements (e.g. signaling pathway and substrate shuttling elements, receptors). Sex hormones, environmental and life-style factors augment or improve the female 'genetic' disadvantage, in ways that are possibly also genetically predetermined. SUMMARY: Women are distinctly different to men with regard to the actions of insulin, the susceptibility to develop insulin resistance, and the response to stimuli that are known to enhance or impair sensitivity to the effects of insulin. Therefore, sex has to be considered when investigating insulin action, metabolic pathways known to be affected by the actions of insulin and diseases that result from abnormalities in insulin action and their treatment.

Diabetes Mellitus, Type 2↗
PubMed2005

Tumor necrosis factor-alpha induces skeletal muscle insulin resistance in healthy human subjects via inhibition of Akt substrate 160 phosphorylation.

Most lifestyle-related chronic diseases are characterized by low-grade systemic inflammation and insulin resistance. Excessive tumor necrosis factor-alpha (TNF-alpha) concentrations have been implicated in the development of insulin resistance, but direct evidence in humans is lacking. Here, we demonstrate that TNF-alpha infusion in healthy humans induces insulin resistance in skeletal muscle, without effect on endogenous glucose production, as estimated by a combined euglycemic insulin clamp and stable isotope tracer method. TNF-alpha directly impairs glucose uptake and metabolism by altering insulin signal transduction. TNF-alpha infusion increases phosphorylation of p70 S6 kinase, extracellular signal-regulated kinase-1/2, and c-Jun NH(2)-terminal kinase, concomitant with increased serine and reduced tyrosine phosphorylation of insulin receptor substrate-1. These signaling effects are associated with impaired phosphorylation of Akt substrate 160, the most proximal step identified in the canonical insulin signaling cascade regulating GLUT4 translocation and glucose uptake. Thus, excessive concentrations of TNF-alpha negatively regulate insulin signaling and whole-body glucose uptake in humans. Our results provide a molecular link between low-grade systemic inflammation and the metabolic syndrome.

Adult↗
PubMed2004

Stable isotope tracer dilution for quantifying very low-density lipoprotein-triacylglycerol kinetics in man.

BACKGROUND & AIM: A number of approaches have been employed in the past to measure very low-density lipoprotein (VLDL) triacylglycerol (TG) kinetics in humans in vivo, varying in the selection of tracer and mode of administration. All, however, make use of labeled TG precursors and more or less complicated mathematical models to derive the kinetic parameters of interest. The aim of the present study was to develop a conceptually straightforward method, based on the traditional tracer infusion technique, for quantifying VLDL-TG production rates in man using stable isotopes. METHOD: Our approach involves ingestion of [U-13C3]glycerol to endogenously label the glycerol in VLDL-TG, plasmapheresis, isolation of the newly 13C-labeled VLDL from plasma, and administration within the next 2-3 days via a primed constant autologous reinfusion. This procedure produces enough tracer for a priming dose plus 2-3 h of infusion. In the physiological conditions examined (basal and hyperglycemic states, fat- and carbohydrate-rich diets), with almost 3-fold ranging VLDL-TG pool sizes, a steady state in plasma VLDL-TG glycerol tracer-to-tracee ratio was readily achieved within 2 h. Consequently, calculations are made according to the isotope dilution principle, thus avoiding assumptions implicit in more complicated models. CONCLUSION: The stable isotope VLDL-TG tracer dilution method offers an alternative and reliable tool for the determination of endogenous VLDL-TG kinetics in man under a variety of metabolic states.

Adult↗
PubMed2004

Are peristaltic pumps as reliable as syringe pumps for metabolic research? Assessment of accuracy, precision, and metabolic kinetics.

Syringe pumps are traditionally used to infuse tracers in metabolic research because they are perceived to be more accurate and precise than peristaltic pumps. This study evaluated the accuracy (actual v programmed infusion rate) and precision (reproducibility of infusion) of a peristaltic pump (Gemini PC 2; IMED, San Diego, CA) and a syringe pump (Model 22; Harvard Apparatus, Natick, MA) for metabolic research. In one protocol, saline delivery was measured in vitro in 5 trials at 4 flow rates: 3, 30, 150, and 300 mL/h. In the second protocol, basal glycerol rate of appearance (Ra) was determined in vivo in 5 women on 2 consecutive days. On day 1, [2-(13C)]glycerol was infused with 1 pump and [1,1,2,3,3-(2H5)]glycerol with the other. On day 2, the opposite pattern was used. The accuracy of the 2 pumps was the same (error approximately 2%). In addition, both the syringe and the peristaltic pumps were very precise, with coefficients of variation (CV) <1% at all flow rates. Glycerol Ra values were the same when tracer was infused with either a syringe or peristaltic pump on day 1 and day 2: 4.1 +/- 1.7 (syringe pump) and 4.2 +/- 1.9 (peristaltic pump) micromol. kg fat mass (FM)(-1). min(-1) on day 1; 4.2 +/- 1.2 (syringe pump) and 4.2 +/- 1.3 (peristaltic pump) micromol. kg FM(-1). min(-1) on day 2. These data demonstrate that both syringe and peristaltic pumps are very accurate and precise across a large range of flow rates. Moreover, the assessment of in vivo substrate kinetics in human subjects is the same when either pump is used to infuse isotope tracers.

Adult↗
PubMed2004

Reconsidering idiopathic CK-elevation.

This study investigated the frequency of persisting, idiopathic creatine-kinase (CK)-elevation, how often the cause of idiopathic CK-elevation could be clarified, and the most frequent causes of idiopathic CK-elevation. Among 28 patients with previously idiopathic CK-elevation, CK remained elevated in 32%. The cause of idiopathic CK-elevation could be determined in 46%. Causes were mitochondriopathy (n = 5), seizure (n = 2), stroke (n = 2), myositis (n = 1), intramuscular-injection (n = 1), alcohol myopathy (n = 1), and pravastátin myopathy (n = 1). In 10 of these patients CK was normal at follow-up. CK-elevation remained idiopathic in 54%. Idiopathic CK-elevation should be comprehensively re-evaluated, even if CK is only slightly elevated or normal at follow-up.

Adult↗
PubMed2003

Excess body fat in men decreases plasma fatty acid availability and oxidation during endurance exercise.

The effect of relative body fat mass on exercise-induced stimulation of lipolysis and fatty acid oxidation was evaluated in 15 untrained men (5 lean, 5 overweight, and 5 obese with body mass indexes of 21 +/- 1, 27 +/- 1, and 34 +/- 1 kg/m2, respectively, and %body fat ranging from 12 to 32%). Palmitate and glycerol kinetics and substrate oxidation were assessed during 90 min of cycling at 50% peak aerobic capacity (VO2 peak) by use of stable isotope-labeled tracer infusion and indirect calorimetry. An inverse relationship was found between %body fat and exercise-induced increase in glycerol appearance rate relative to fat mass (r2 = 0.74; P < 0.01). The increase in total fatty acid uptake during exercise [(micromol/kg fat-free mass) x 90 min] was approximately 50% smaller in obese (181 +/- 70; P < 0.05) and approximately 35% smaller in overweight (230 +/- 71; P < 0.05) than in lean (354 +/- 34) men. The percentage of total fatty acid oxidation derived from systemic plasma fatty acids decreased with increasing body fat, from 49 +/- 3% in lean to 39 +/- 4% in obese men (P < 0.05); conversely, the percentage of nonsystemic fatty acids, presumably derived from intramuscular and possibly plasma triglycerides, increased with increasing body fat (P < 0.05). We conclude that the lipolytic response to exercise decreases with increasing adiposity. The blunted increase in lipolytic rate in overweight and obese men compared with lean men limits the availability of plasma fatty acids as a fuel during exercise. However, the rate of total fat oxidation was similar in all groups because of a compensatory increase in the oxidation of nonsystemic fatty acids.

Adipose Tissue↗
PubMed2003

Effect of sex and obesity on basal VLDL-triacylglycerol kinetics.

BACKGROUND: Plasma fatty acid availability is a major regulator of VLDL-triacylglycerol production. Basal whole-body lipolysis is higher in women than in men and is higher in persons with abdominal obesity than in lean individuals. OBJECTIVE: Our goal was to determine whether sex and abdominal obesity affect VLDL-triacylglycerol kinetics. We hypothesized that basal VLDL-triacylglycerol production would be greater in women than in men and greater in obese than in lean subjects. DESIGN: VLDL-triacylglycerol kinetics were measured in 20 lean (10 men, 10 women; body mass index, in kg/m(2): 23 +/- 1) and 20 abdominally obese (10 men, 10 women; body mass index: 35 +/- 1) subjects by using a bolus injection of [(2)H(5)]glycerol and compartmental modeling analysis. RESULTS: The rate of VLDL-triacylglycerol secretion was greater in the lean women than in the lean men (5.1 +/- 0.7 and 2.6 +/- 0.3 micro mol x L plasma(-1) x min(-1), respectively; P < 0.002). Obesity was associated with increased VLDL-triacylglycerol secretion in the men (P < 0.001) but not in the women, which resulted in greater rates of VLDL-triacylglycerol secretion in the obese men than in the obese women (6.8 +/- 0.5 and 5.0 +/- 0.5 micro mol x L plasma(-1) x min(-1), respectively; P < 0.05). The clearance of VLDL-triacylglycerol from plasma was greater (P < 0.05) in the lean women than in the lean men (42 +/- 7 and 27 +/- 4 mL plasma/min, respectively) or in the obese men and obese women (28 +/- 3 and 20 +/- 4 mL plasma/min, respectively). The plasma VLDL-triacylglycerol concentration was directly related to the rate of VLDL-triacylglycerol secretion in the men (R(2) = 0.79, P < 0.001) and inversely related to VLDL-triacylglycerol clearance in the women (R(2) = 0.84, P<0.001). CONCLUSION: Sex and obesity have independent effects on basal VLDL-triacylglycerol kinetics.

Abdomen↗
PubMed2003

Essential amino acids are primarily responsible for the amino acid stimulation of muscle protein anabolism in healthy elderly adults.

BACKGROUND: Nutritional supplementation may be used to treat muscle loss with aging (sarcopenia). However, if physical activity does not increase, the elderly tend to compensate for the increased energy delivered by the supplements with reduced food intake, which results in a calorie substitution rather than supplementation. Thus, an effective supplement should stimulate muscle anabolism more efficiently than food or common protein supplements. We have shown that balanced amino acids stimulate muscle protein anabolism in the elderly, but it is unknown whether all amino acids are necessary to achieve this effect. OBJECTIVE: We assessed whether nonessential amino acids are required in a nutritional supplement to stimulate muscle protein anabolism in the elderly. DESIGN: We compared the response of muscle protein metabolism to either 18 g essential amino acids (EAA group: n = 6, age 69 +/- 2 y; +/- SD) or 40 g balanced amino acids (18 g essential amino acids + 22 g nonessential amino acids, BAA group; n = 8, age 71 +/- 2 y) given orally in small boluses every 10 min for 3 h to healthy elderly volunteers. Muscle protein metabolism was measured in the basal state and during amino acid administration via L-[ring-(2)H(5)]phenylalanine infusion, femoral arterial and venous catheterization, and muscle biopsies. RESULTS: Phenylalanine net balance (in nmol x min(-1). 100 mL leg volume(-1)) increased from the basal state (P < 0.01), with no differences between groups (BAA: from -16 +/- 5 to 16 +/- 4; EAA: from -18 +/- 5 to 14 +/- 13) because of an increase (P < 0.01) in muscle protein synthesis and no change in breakdown. CONCLUSION: Essential amino acids are primarily responsible for the amino acid-induced stimulation of muscle protein anabolism in the elderly.

Aged↗
PubMed2003

What does the measurement of whole-body fatty acid rate of appearance in plasma by using a fatty acid tracer really mean?

We evaluated the validity of using a single fatty acid tracer to assess total plasma long-chain free fatty acid (FFA) kinetics and the relationship between the rate of appearance (R(a)) of fatty acids in plasma and the fatty acid composition of adipose tissue triglyceride (TG). A mixture of [(13)C]-labeled myristate, palmitate, stearate, oleate, and linoleate was infused in healthy men during basal conditions and during conditions that stimulate (epinephrine infusion) and inhibit (insulin infusion) lipolysis of adipose tissue TGs. Calculated total FFA, R(a) based on palmitate, oleate, or linoleate tracers, was within 15% of the measured sum of the individual fatty acid R(a) under all conditions, whereas stearate and myristate tracers consistently underestimated and overestimated total FFA R(a), respectively. The fatty acid R(a) profile closely matched the fatty acid profile of subcutaneous adipose tissue TGs during epinephrine infusion, but not during basal conditions and insulin infusion. Our data support the common practice of using labeled palmitate or oleate as fatty acid tracers for assessing total plasma FFA kinetics and suggest that a source of lipids other than adipose tissue TG release fatty acids into the systemic circulation.

Adipose Tissue↗
PubMed2002

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

The effects of obesity and weight loss on lipoprotein kinetics were evaluated in six lean women [body mass index (BMI): 21 +/- 1 kg/m(2)] and seven women with abdominal obesity (BMI: 36 +/- 1 kg/m(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 approximately 40% (from 0.41 +/- 0.05 to 0.23 +/- 0.03 micromol x kg fat-free mass(-1) x min(-1); P < 0.05). The relative decline in VLDL-TG produced from nonsystemic fatty acids, derived from intraperitoneal and intrahepatic TG, was greater (61 +/- 7%) than the decline in VLDL-TG produced from systemic fatty acids, predominantly derived from subcutaneous TG (25 +/- 8%; P < 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.

Abdomen↗