Fat redistribution following suction lipectomy: defense of body fat and patterns of restoration.

No randomized studies in humans have examined whether fat returns after removal or where it returns. We undertook a prospective, randomized-controlled trial of suction lipectomy in nonobese women to determine if adipose tissue (AT) is defended and if so, the anatomic pattern of redistribution. Healthy women with disproportionate AT depots (lower abdomen, hips, or thighs) were enrolled.

Leptin increases skeletal muscle lipoprotein lipase and postprandial lipid metabolism in mice.

The ability of leptin to preserve lean tissue during weight loss may be in part due to differences in nutrient partitioning. Because lipoprotein lipase (LPL) plays a key role in partitioning lipid nutrients, this study was conducted to test the hypothesis that leptin would modify the tissue-specific regulation of LPL and result in increased lipid oxidation and decreased storage. The effects of daily intraperitoneal leptin injections (2 mg/kg body weight) over 2 weeks on LPL activity and postprandial lipid metabolism were tested in both wild-type (WT), leptin-deficient ob/ob obese mice and mice pair fed to the leptin-treated mice.

The metabolic syndrome.

The "metabolic syndrome" (MetS) is a clustering of components that reflect overnutrition, sedentary lifestyles, and resultant excess adiposity. The MetS includes the clustering of abdominal obesity, insulin resistance, dyslipidemia, and elevated blood pressure and is associated with other comorbidities including the prothrombotic state, proinflammatory state, nonalcoholic fatty liver disease, and reproductive disorders. Because the MetS is a cluster of different conditions, and not a single disease, the development of multiple concurrent definitions has resulted.

Increased thermogenic responsiveness to intravenous beta-adrenergic stimulation in habitually exercising humans is not related to skeletal muscle beta2-adrenergic receptor density.

Habitually exercising adults demonstrate greater thermogenic responsiveness to beta-adrenergic receptor (beta-AR) stimulation compared with their sedentary peers, but the molecular mechanisms involved are unknown. To determine the possible role of increased beta-AR density, we studied 32 healthy adults: 17 habitual aerobic exercisers (age 45 +/- 5 years, 11 males) and 15 sedentary (49 +/- 5 years, 7 males). Maximal oxygen uptake (43.

Thermic effect of food and beta-adrenergic thermogenic responsiveness in habitually exercising and sedentary healthy adult humans.

The thermic effect of food (TEF) is an important physiological determinant of total daily energy expenditure (EE) and energy balance. TEF is believed to be mediated in part by sympathetic nervous system activation and consequent beta-adrenergic receptor (beta-AR) stimulation of metabolism. TEF is greater in habitually exercising than in sedentary adults, despite similar postprandial sympathetic nervous system activation.

Thermogenic responsiveness to beta-adrenergic stimulation is augmented in exercising versus sedentary adults: role of oxidative stress.

Beta-adrenergic receptor (beta-AR) modulation of resting and postprandial energy expenditure (EE) is augmented in regularly exercising compared with sedentary adults, but the underlying physiological mechanisms are unknown. Differences in thermogenic responsiveness to beta-AR stimulation, perhaps secondary to reactive oxygen species (ROS) bioactivity, may be involved. To determine habitual exercise-related differences in beta-AR thermogenic responsiveness and the possible influence of ROS, we measured the percentage increase in EE (DeltaEE%; indirect calorimetry, ventilated hood method) above resting EE in response to non-specific beta-AR stimulation (intravenous isoproterenol (isoprenaline): 6, 12 and 24 ng (kg fat-free mass)-1 min-1) in 25 sedentary (11 males; 51+/-4 years; body mass index 25.

Thermogenic responsiveness to nonspecific beta-adrenergic stimulation is not related to genetic variation in codon 16 of the beta2-adrenergic receptor.

Stimulation of beta-adrenergic receptors (beta-AR) by the sympathetic nervous system (SNS) modulates energy expenditure (EE), but substantial interindividual variability is observed. We determined whether the thermogenic response to beta-AR stimulation is related to genetic variation in codon 16 of the beta(2)-AR, a biologically important beta-AR polymorphism, and whether differences in SNS activity (i.e.