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PubMed2003

Moderate alcohol consumption, dietary fat composition, and abdominal obesity in women: evidence for gene-environment interaction.

We examined relationships among alcohol intake, dietary fat composition, and total body fat (TBF) and central abdominal fat (CAF), independent of genetic confounders, and evaluated the modulating effect of genetic susceptibility. We studied 334 female twins (57.7 +/- 6.7 yr) after excluding dietary underreporters. Diet was assessed by Food-Frequency Questionnaire and body fat by dual-energy x-ray absorptiometry. Moderate alcohol consumers (12-17.9 g/d) had less TBF (20.6 +/- 5.6 vs. 24.8 +/- 8.4 kg, P = 0.03) and CAF (1.2 +/- 0.6 vs. 1.6 +/- 0.7 kg, P = 0.03) than abstainers. In multiple regression, alcohol consumption remained independently associated with body fat distribution. In cotwin case-control (monozygotic twin) analysis, moderate alcohol consumption accounted for 300 g less CAF, independent of genetic and other environmental factors. Gene-environment interaction analysis indicated that this association was limited to subjects at high genetic risk of abdominal obesity. There was no relationship between dietary fat composition and adiposity. However, in women at low genetic risk of abdominal obesity, subjects with polyunsaturated fat intakes in the highest tertile had about 50% less CAF than subjects with intakes in the lowest tertile (0.9 +/- 0.4 vs. 1.6 +/- 0.4 kg, P = 0.0007), an association absent in subjects with high genetic risk. In conclusion, genetic risk modulates relationships between dietary factors and adiposity. Lower abdominal fat may mediate associations between dietary intake and type 2 diabetes risk.

Abdomen↗
PubMed2004

Abdominal obesity and dyslipidemia in the metabolic syndrome: importance of type 2 diabetes and familial combined hyperlipidemia in coronary artery disease risk.

Regional body fat distribution has an important influence on metabolic and cardiovascular risk factors. Increased abdominal (visceral) fat accumulation is a risk factor for coronary artery disease (CAD), dyslipidemia, hypertension, stroke, and type 2 diabetes. The recent emphasis on treatment of the dyslipidemia of the metabolic syndrome (hypertriglyceridemia, reduced high-density lipoprotein, and increased small, dense low-density lipoprotein particle number) has compelled practitioners to consider lipid-lowering therapy in a greater number of their patients, as one in two individuals over age 50 has the metabolic syndrome. Individuals with the metabolic syndrome typically have normal low-density lipoprotein cholesterol levels, and current lipid-lowering guidelines may underestimate their cardiovascular risk. Two subgroups of patients with the metabolic syndrome are at particularly high risk for premature CAD. One, individuals with type 2 diabetes, accounts for 20-30% of early cardiovascular disease. The second, familial combined hyperlipidemia, accounts for an additional 10-20% of premature CAD. Familial combined hyperlipidemia is characterized by the metabolic syndrome in addition to a disproportionate elevation of apolipoprotein B levels. The measurement of fasting glucose and apolipoprotein B, in addition to the fasting lipid profile, can help to estimate CAD risk in patients with the metabolic syndrome.

Abdomen↗
PubMed2004

Expression and activity of 20alpha-hydroxysteroid dehydrogenase (AKR1C1) in abdominal subcutaneous and omental adipose tissue in women.

We examined the expression and activity of 20alpha-hydroxysteroid dehydrogenase (20alpha-HSD) in abdominal adipose tissue in women. This recently characterized enzyme from the aldoketoreductase 1C family is responsible for the conversion of progesterone into 20alpha-hydroxyprogesterone. Abdominal sc (SC) and omental (OM) adipose tissue biopsies were obtained from a sample of 32 women aged 47.7 +/- 5.9 yr (body mass index 27.6 +/- 5.0 kg/m(2)) undergoing abdominal hysterectomies. Body composition and body fat distribution measurements were performed before the surgery by dual-energy x-ray absorptiometry and computed tomography, respectively. The expression of 20alpha-HSD was determined by real-time RT-PCR, and its activity was measured in whole-tissue homogenates. mRNA and activity of the enzyme were detected in both the SC and OM fat depots, the two measures being significantly higher in the SC compartment. Women characterized by a visceral adipose tissue area of 100 cm(2) or greater had an increased 20alpha-HSD conversion rate in their OM adipose tissue, compared with women without visceral obesity (13.99 +/- 2.07 vs. 7.92 +/- 0.83 fmol/microg protein per 24 h, P < 0.05). Accordingly, a positive correlation was found between OM adipose tissue 20alpha-HSD activity and computed tomography-measured visceral adipose tissue area (r = 0.36, P < 0.05). Significant positive correlations were also found between OM 20alpha-HSD activity and OM adipocyte diameter (r = 0.49, P < 0.05) and OM adipose tissue LPL activity (r = 0.36, P = 0.06). In conclusion, 20alpha-HSD activity and mRNA were detected in SC and OM adipose tissue in women, and OM 20alpha-hydroxylation of progesterone was highest in women with visceral obesity. Additional studies are required to establish whether local conversion of progesterone may impact on the metabolism and function of adipocytes located within the abdominal cavity.

20-Hydroxysteroid Dehydrogenases↗
PubMed2004

Antiretroviral treatment reduces very-low-density lipoprotein and intermediate-density lipoprotein apolipoprotein B fractional catabolic rate in human immunodeficiency virus-infected patients with mild dyslipidemia.

The relationship between antiretroviral treatment of HIV infection, body fat distribution, insulin resistance, and very-low-density lipoprotein (VLDL) and intermediate-density lipoprotein (IDL) apolipoprotein-B (apoB) kinetics was investigated in 55 HIV-infected patients taking two nucleoside analogs plus either a protease inhibitor (n = 15) or a nonnucleoside reverse transcriptase inhibitor (n = 25), 15 antiretroviral therapy-naive patients, and 12 HIV-negative controls. Compared with the controls, high-density lipoprotein cholesterol was reduced in all groups (P < 0.01). Plasma triglyceride was increased in patients taking protease inhibitors (P < 0.05). VLDL and IDL apoB fractional catabolic rate (FCR) was lower in all treatment groups (P < 0.05) compared with controls. Trunk fat, VLDL apoB absolute secretion rate, and insulin resistance were not different between groups. Peripheral fat was lower in the treated patients (P < 0.05) and correlated with duration of therapy (r = -0.55; P < 0.001). There was a positive correlation between peripheral fat and VLDL apoB FCR (P = 0.002) and IDL apoB FCR (P = 0.002) and a negative correlation with VLDL apoB pool size, VLDL cholesterol, and triglyceride (P < 0.03; P < 0.01; P < 0.002). These results suggest that mild dyslipidemia resulting from antiretroviral therapy is caused by a decrease in VLDL and IDL apoB FCR, which is associated with a loss of peripheral fat.

Adult↗
PubMed2006

Opposing influences of prenatal and postnatal growth on the timing of menarche.

CONTEXT AND OBJECTIVE: Menarche is a milestone of reproductive development, and its timing may be differentially influenced by the growth conditions before birth and those between birth and puberty. The present study explored the relationships among menarcheal timing and markers of prenatal and midchildhood growth in healthy Australian girls. SETTING, DESIGN, AND PATIENTS: A total of 156 girls aged 8 yr from a birth cohort of full-term babies had height, weight, and waist circumference measured. One hundred three girls had dual x-ray absorptiometry performed and blood analyzed for insulin, leptin, IGF-I, estradiol, and dehydroepiandrosterone sulfate levels. Girls were followed up at age 15 yr and their age of menarche was recorded. MAIN OUTCOME MEASURES: Measures included age of menarche; birth weight and birth length; height, weight, waist circumference, and body composition by dual x-ray absorptiometry; and plasma insulin, leptin, IGF-I, estradiol, and dehydroepiandrosterone sulfate at age 8 yr. RESULTS: Girls with earlier menarche were light and long at birth and had higher total and central adiposity and IGF-I and estradiol levels in midchildhood, compared with those with later menarche. Age of menarche was best predicted by combining size at birth and body mass index z score at age 8 yr (r2 = 0.12; P < 0.001). CONCLUSIONS: The timing of menarche appears to be influenced in opposing directions by pre- and postnatal growth. Menarche was found to occur earlier in girls who were long and light at birth and who had a higher fat mass and circulating IGF-I in childhood. These findings may partly explain ethnic differences and secular trends in the age of menarche.

Adolescent↗
PubMed2006

Influence of serum leptin on weight and body fat growth in children at high risk for adult obesity.

OBJECTIVE: Our objective was to examine serum leptin prospectively as a predictor of weight and body fat growth in children at high risk for adult obesity. We hypothesized that leptin measurements would be positively associated with increased growth of adipose tissue because children with high baseline leptin for their body fat mass have greater leptin resistance and thus would have greater susceptibility to weight gain. METHODS: Children ages 6-12 yr at high risk for adult obesity because of early-onset childhood overweight and/or parental overweight were recruited from 1996-2004. Growth in body mass index (BMI) was studied in 197 children, and growth in total body fat mass was examined in 149 children over an average follow-up interval of 4.4 yr (range, 1-8 yr). Longitudinal analyses accounted for sex, race, socioeconomic status, initial body composition, age, skeletal age, and physical activity and included all available interim visits for each individual so that a total of 982 subject visits were included in the analysis. RESULTS: At baseline, 43% of children studied were overweight (BMI > or = 95th percentile); during follow-up, an additional 14% became overweight. Independent of initial body composition, baseline leptin was a statistically significant positive predictor of increased BMI (P = 0.0147) and increased total body fat mass (P < 0.007). CONCLUSIONS: High serum leptin, independent of body fat, may be an indicator of increased leptin resistance, which predisposes children at high risk for adult obesity to somewhat greater growth in weight and body fat during childhood.

Adipose Tissue↗
PubMed1989

Clinical and hormonal characteristics of obese amenorrheic hyperandrogenic women before and after weight loss.

We studied a group of obese hyperandrogenic amenorrheic women to determine the effects of weight loss on anthropometry, hormonal status, menstrual cycles, ovulation, and fertility. Fourteen women had polycystic ovaries, two the hyperandrogenism-insulin resistance-acanthosis nigricans syndrome, one hirsutism of adrenal origin, and three idiopathic chronic anovulation. The duration of amenorrhea before the study ranged from 3-17 months [mean, 8.6 +/- 4.5 (+/- SD)]. All women ate a hypocaloric diet for a period of 8.0 +/- 2.4 months. Weight loss ranged from 4.8 to 15.2 kg (mean, 9.7 +/- 3.1 kg; 1.35 +/- 0.56 kg/month) and the waist to hip ratio, which was used as a measurement of body fat distribution, decreased from 0.86 +/- 0.1 to 0.81 +/- 0.06 (P less than 0.0001). The women's mean plasma testosterone and LH concentrations decreased significantly (P less than 0.001 and P less than 0.005, respectively). A significant positive correlation was found between the decreases in plasma testosterone levels and the decreases in glucose-stimulated insulin levels. Moreover, the decreases in the waist to hip ratio correlated positively with the decreases in glucose-stimulated insulin levels and inversely with the decreases in plasma 17 beta-estradiol. No relationships were found between weight loss and the changes in plasma insulin, steroid, and gonadotropin concentrations. The responsiveness to the weight reduction program was evaluated by comparing the number of menstrual cycles during the study period with the number reported before it. Eight women had significantly improved menstrual cyclicity (responders), while 12 did not (nonresponders). The clinical characteristics and hormone values were similar in responder and nonresponder women. In the group as a whole, 33% of the menstrual cycles during the study were ovulatory, and 4 pregnancies occurred. Hirsutism improved significantly in more than half of the women, as did acanthosis nigricans when present. We conclude that weight loss is beneficial in all obese hyperandrogenic women regardless of the presence of polycystic ovaries, the degree of hyperandrogenism, and the degree and distribution of obesity.

Adult↗
PubMed1992

Insulin regulation of insulin-like growth factor binding protein-1 in obese and nonobese humans.

Insulin is the principal regulator of hepatic insulin-like growth factor binding protein-1 (IGFBP-1) production, mediating the rapid decrease in plasma IGFBP-1 in response to nutritional intake. In this study, we defined IGFBP-1 regulation by insulin in upper and lower body obesity, conditions associated with insulin resistance and chronic hyperinsulinemia. Overnight postabsorptive IGFBP-1 levels in obese and nonobese women showed an inverse, nonlinear relationship with plasma insulin concentrations. Maximum suppression of IGFBP-1 was seen at 70-90 pmol/L plasma insulin. Both groups of obese women had mean fasting plasma insulin concentrations above this threshold level and, consequently, markedly suppressed IGFBP-1 levels. To assess the dynamics of insulin regulated IGFBP-1, 10 obese and 8 nonobese women were studied during sequential saline infusion (0-90 min), hyperinsulinemia (insulin infusion; 90-210 min) and hypoinsulinemia (somatostatin + GH infusion; 210-330 min). Insulin infusion rapidly decreased plasma IGFBP-1 levels in nonobese subjects (60% decrease in 2 h), but had little or no further suppressive effect in obese subjects. Complete insulin withdrawal resulted in a significant rise in plasma IGFBP-1 concentrations in all subjects, but the response was blunted in obese compared to nonobese groups. In contrast to plasma IGFBP-1, IGF-I concentrations did not vary during hyper- and hypoinsulinemic infusion periods and were not significantly different between groups. Basal GH levels were significantly higher in nonobese when compared to obese women, but did not change with infusions. In conclusion, low IGFBP-1 levels in obesity are related to elevated insulin levels which are, in turn, related to body fat distribution and insulin resistance. The chronically depressed levels of IGFBP-1 may promote IGF bioactivity as well as its feedback regulation of GH secretion, thus contributing to the metabolic and mitogenic consequences of obesity. In addition, our findings imply that hepatic insulin sensitivity in terms of IGFBP-1 production is preserved despite peripheral insulin resistance in obesity.

Adult↗
PubMed1997

Troglitazone improves defects in insulin action, insulin secretion, ovarian steroidogenesis, and fibrinolysis in women with polycystic ovary syndrome.

Women with polycystic ovary syndrome (PCOS) are characterized by defects in insulin action, insulin secretion, ovarian steroidogenesis, and fibrinolysis. We administered the insulin-sensitizing agent troglitazone to 13 obese women with PCOS and impaired glucose tolerance to determine whether attenuation of hyperinsulinemia ameliorates these defects. All subjects had oligomenorrhea, hirsutism, polycystic ovaries, and hyperandrogenemia. Before and after treatment with troglitazone (400 mg daily for 12 weeks), all had 1) a GnRH agonist (leuprolide) test, 2) a 75-g oral glucose tolerance test, 3) a frequently sampled iv glucose tolerance test to determine the insulin sensitivity index and the acute insulin response to glucose, 4) an oscillatory glucose infusion to assess the ability of the beta-cell to entrain to glucose as quantitated by the normalized spectral power for the insulin secretion rate, and 5) measures of fibrinolytic capacity [plasminogen activator inhibitor type 1 (PAI-1) and tissue plasminogen activator]. There was no change in body mass index (39.9 +/- 1.4 vs. 40.2 +/- 1.4 kg/m2) or body fat distribution after treatment. Both the fasting (91 +/- 3 vs. 103 +/- 3 mg/dL; P < 0.001) and 2 h (146 +/- 8 vs. 171 +/- 6 mg/dL; P < 0.02) plasma glucose concentrations during the oral glucose tolerance test declined significantly. There was a concordant reduction in glycosylated hemoglobin to 5.7 +/- 0.1 from a pretreatment level of 6.1 +/- 0.1% (P < 0.03). Insulin sensitivity increased from 0.58 +/- 0.14 to 0.95 +/- 0.26 10(-5) min-1/pmol.L (P < 0.01) after treatment as did the disposition index (745 +/- 135 vs. 381 +/- 96; P < 0.05). The ability of the beta-cell to appropriately detect and respond to an oscillatory glucose infusion improved significantly after troglitazone treatment; the normalized spectral power for the insulin secretion rate increased to 5.9 +/- 1.1 from 4.3 +/- 0.8 (P < 0.05). Basal levels of total testosterone (109.3 +/- 15.2 vs. 79.4 +/- 9.8 ng/dL; P < 0.05) and free testosterone (33.3 +/- 4.0 vs. 21.2 +/- 2.6 pg/mL; P < 0.01) declined significantly after troglitazone treatment. Leuprolide-stimulated levels of 17-hydroxyprogesterone, androstenedione, and total testosterone were significantly lower posttreatment compared to pretreatment. The reduction in androgen levels occurred independently of any changes in gonadotropin levels. A decreased functional activity of PAI-1 in blood (from 12.7 +/- 2.8 to 6.3 +/- 1.4 AU/mL P < 0.05) was associated with a decreased concentration of PAI-1 protein (from 64.9 +/- 9.1 to 44.8 +/- 6.1 ng/mL; P < 0.05). No change in the functional activity of tissue plasminogen activator (from 5.3 +/- 0.4 to 5.1 +/- 0.5 IU/mL) was observed despite a decrease in its concentration (from 9.6 +/- 0.9 to 8.2 +/- 0.7 ng/mL; P < 0.05). The marked reduction in PAI-1 could be expected to improve the fibrinolytic response to thrombosis in these subjects. We conclude that administration of troglitazone to women with PCOS and impaired glucose tolerance ameliorates the metabolic and hormonal derangements characteristic of the syndrome. Troglitazone holds potential as a useful primary or adjunctive treatment for women with PCOS.

Adult↗
PubMed1999

Cortisol metabolism in healthy young adults: sexual dimorphism in activities of A-ring reductases, but not 11beta-hydroxysteroid dehydrogenases.

Cortisol is metabolized irreversibly by A-ring reductases (5alpha- and 5beta-reductases) and reversibly (to cortisone) by 11beta-hydroxysteroid dehydrogenases (11betaHSDs). In rats, estradiol down-regulates 11betaHSD1 expression. In humans, ratios of urinary cortisol/cortisone metabolites differ in men and women. In this study, urinary cortisol metabolites and hepatic 11betaHSD1 activity were measured in healthy young men and women at different phases of the menstrual cycle. Ten men and 10 women with regular menstrual cycles collected a 24-h urine sample, took 250 microg oral dexamethasone at 2300 h, took 25 mg oral cortisone at 0900 h (after fasting), and had blood sampled for plasma cortisol estimation over the subsequent 150 min. Women repeated the tests in random order in menstrual, follicular, and luteal phases. Women excreted disproportionately less A-ring-reduced metabolites of cortisol [median 5alpha-tetrahydrocortisol, 1811 (interquartile range, 1391-2300) microg/day in menstrual phase vs. 2723 (interquartile range, 2454-3154) in men (P = 0.01); 5beta-tetrahydrocortisol, 1600 (interquartile range, 1419-1968) vs. 2197 (interquartile range, 1748-2995; P = 0.03)] but similar amounts of cortisol, cortisone, and tetrahydrocortisone. Analogous differences were observed in urinary excretion of androgen metabolites. Conversion of cortisone to cortisol on hepatic first pass metabolism was not different (peak plasma cortisol, 733 +/- 60 nmol/L in women vs. 684 +/- 53 nmol/L in men; mean +/- SEM; P = 0.55). There were no differences in cortisol or androgen metabolism between phases of the menstrual cycle. We conclude that sexual dimorphism in cortisol metabolite excretion is attributable to less A-ring reduction of cortisol in women, rather than less reactivation of cortisone to cortisol by 11betaHSD1. This difference is not influenced acutely by gonadal steroids. 11BetaHSD1 has been suggested to modulate insulin sensitivity and body fat distribution, but caution must be exercised in extrapolating inferences about its regulation from rodents to man. A-Ring reductases may have an equally important influence on metabolic clearance of cortisol and intracellular cortisol concentrations.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed2002

Absence of Cushingoid phenotype in a patient with Cushing's disease due to defective cortisone to cortisol conversion.

Cushing's syndrome invariably presents with a classical phenotype comprising central adiposity, prominence of dorsal, supraclavicular and temporal fat pads, bruising, abdominal striae, proximal myopathy, and hypertension. We report the case of a 20-yr-old student with pituitary-dependent Cushing's syndrome who was spared this classical phenotype because of a defect in the peripheral conversion of cortisone to cortisol. She presented to her general practitioner with secondary amenorrhea. Clinical examination revealed normal fat distribution (body mass index, 20.9 kg/m(2)), absence of hirsutism, myopathy, or bruising; her blood pressure ranged from 115/70 to 122/82 mm Hg. She was investigated for biochemical hypercortisolemia because of a mildly elevated random circulating cortisol (serum cortisol, 661 nmol/liter). Cushing's syndrome was confirmed on the basis of repeatedly elevated urinary free cortisols (831-1049; reference range, <350 nmol/24 h), failure of low-dose dexamethasone suppression (611 nmol/liter) and loss of circadian cortisol secretion. Investigations suggested Cushing's disease; there was suppression after high-dose dexamethasone (<20 nmol/liter) and a 950% increase in ACTH after stimulation with CRH. Pituitary magnetic resonance imaging revealed a 3-mm adenoma within the pituitary gland. Urinary corticosteroid metabolites were analyzed by gas chromatography-mass spectrometry and demonstrated a decreased THF+allo-THF/THE ratio of 0.66 (mean +/- SE in Cushing's disease, 1.74 +/- 0.24) suggesting a defect in 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1), an enzyme that converts the inactive glucocorticoid cortisone to active cortisol. Transphenoidal microadenomectomy was performed, and histology confirmed the diagnosis of a corticotroph adenoma. Postoperatively, serum cortisol was undetectable and replacement therapy was commenced. Subsequent investigations revealed a significantly impaired ability to convert an oral dose of cortisone acetate (25 mg) to cortisol, reduced serum cortisol to cortisone ratios, and a reduced serum half-life for cortisol (57.3 min). These results provide strong evidence for a partial defect in 11beta-HSD1 activity and concomitant increase in cortisol clearance rate. We have described a case of Cushing's disease that failed to present with a classical phenotype, and we postulate that this is due to a partial defect of 11beta-HSD1 activity, the defect in cortisone to cortisol conversion increasing cortisol clearance and thus protecting the patient from the effects of cortisol excess. This observation may help to explain individual susceptibility to the adverse effects of glucocorticoids.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed2006

Seasonal modulation of sickness behavior in free-living northwestern song sparrows (Melospiza melodia morphna).

A variety of vertebrate species modulate immune function on a seasonal basis to cope with seasonal energy deficits and competing life-history demands, such as reproduction. Most studies to date have focused upon seasonal variation of cellular and humoral immunity, while neglecting behavioral responses to infection. These behavioral strategies are collectively termed sickness behaviors and are hypothesized to divert energy away from normal activities to combat and overcome infection. Sickness behavior can be triggered experimentally by injecting bacterial lipopolysaccharide (LPS). In this study, we provide the first evidence for seasonal modulation of sickness behavior in a free-living animal. Male song sparrows of western Washington state (Melospiza melodia morphna) are sedentary and territorial year round, except for a brief time during molt. Treatment with LPS decreased territorial aggressive behavior of males in the winter (nonbreeding), but not in the spring (breeding). Subjects were recaptured approx. 25 h after treatment. Recaptured LPS males in the winter lost more body mass than saline-injected controls while LPS males in the spring did not. These data indicate that birds in breeding condition were relatively insensitive to the effects of LPS. On a proximate level, suppression of sickness behavior during breeding is likely mediated by seasonal differences in energy allocation, as wintering sparrows were significantly heavier and had larger subcutaneous fat reserves and lower baseline corticosterone levels than breeding birds. Ultimately, suppression of sickness behavior may represent an allocation strategy to balance current reproductive opportunities with the life-history costs of self-defense.

Aggression↗
PubMed2004

Overweight athlete: fact or fiction?

Maintaining appropriate body weight is important for athletic performance. Body mass index (BMI) is commonly used to classify an individual's body weight. However, in the case of athletes, who may have a high body weight due to higher lean body mass, BMI may lead to misclassification of the athlete as overweight or obese. Thus, both BMI and body composition assessment should be conducted before determining if an athlete is overweight or obese. Body weight goals of athletes should be determined for each athlete, based on the requirements of the sport, the athlete's body size and shape, and in consultation with the athlete, coaches, and trainers. Safe weight loss goals should be established on an individual basis. Athletes, coaches, and trainers should work closely with individuals who have training in nutrition (registered dietitians) to set appropriate weight goals and to develop weight management protocols that promote healthy eating.

Body Composition↗
PubMed2006

Ablation of PGC-1beta results in defective mitochondrial activity, thermogenesis, hepatic function, and cardiac performance.

The transcriptional coactivator peroxisome proliferator-activated receptor-gamma coactivator-1beta (PGC-1beta) has been implicated in important metabolic processes. A mouse lacking PGC-1beta (PGC1betaKO) was generated and phenotyped using physiological, molecular, and bioinformatic approaches. PGC1betaKO mice are generally viable and metabolically healthy. Using systems biology, we identified a general defect in the expression of genes involved in mitochondrial function and, specifically, the electron transport chain. This defect correlated with reduced mitochondrial volume fraction in soleus muscle and heart, but not brown adipose tissue (BAT). Under ambient temperature conditions, PGC-1beta ablation was partially compensated by up-regulation of PGC-1alpha in BAT and white adipose tissue (WAT) that lead to increased thermogenesis, reduced body weight, and reduced fat mass. Despite their decreased fat mass, PGC1betaKO mice had hypertrophic adipocytes in WAT. The thermogenic role of PGC-1beta was identified in thermoneutral and cold-adapted conditions by inadequate responses to norepinephrine injection. Furthermore, PGC1betaKO hearts showed a blunted chronotropic response to dobutamine stimulation, and isolated soleus muscle fibres from PGC1betaKO mice have impaired mitochondrial function. Lack of PGC-1beta also impaired hepatic lipid metabolism in response to acute high fat dietary loads, resulting in hepatic steatosis and reduced lipoprotein-associated triglyceride and cholesterol content. Altogether, our data suggest that PGC-1beta plays a general role in controlling basal mitochondrial function and also participates in tissue-specific adaptive responses during metabolic stress.

Adipose Tissue, Brown↗
PubMed2001

Sleep-related breathing disorders in adolescents aged 12 to 16 years : clinical and polygraphic findings.

STUDY OBJECTIVES: To determine the frequency, symptoms, and polygraphic features of sleep-related breathing disorders (SRBD) in adolescents aged 12 to 16 years. DESIGN: Cross-sectional study. SETTING: Randomly selected secondary schools in the city of Seville, SPAIN: PARTICIPANTS: A general population sample of adolescents (n = 101; mean [+/- SD] age, 13.2 +/- 0.8 years). INTERVENTIONS: An 82-item questionnaire regarding anthropometric data and nocturnal and daytime symptoms suggestive of SRBD was administered. Symptoms were evaluated according to a 4-point frequency scale. Snorers answered "sometimes" or "often" in the question about snoring, and nonsnorers answered "never" or "rarely." All subjects underwent an overnight cardiorespiratory polygraphy at home. RESULTS: Twenty-nine percent of the subjects were snorers. Excessive daytime sleepiness was present in 14% of subjects, and sleep apnea was present in 3%. Polygraphy showed a respiratory disturbance index > or = 10 in 18 subjects (17.8%), but concurrent symptoms highly suggestive of SRBD were found in only 2 subjects (1.9%). Snorers had higher waist-to-hip ratios and a higher frequency of witnessed apnea or labored breathing as well as higher values of respiratory events as compared with nonsnorers. However, oximetry data were similar in both groups. CONCLUSIONS: In a nonselected group of adolescents aged 12 to 16 years, the frequency of symptoms potentially associated with SRBD was similar to that reported for younger children. Snoring was associated with a higher occurrence of other nocturnal symptoms, a more central pattern of body fat distribution, and a higher respiratory disturbance index as compared with nonsnorers. Although polygraphic abnormalities were mild, two cases of probable SRBD were found with a prevalence rate of 1.9%.

Adolescent↗
PubMed2000

How obesity develops: insights from the new biology.

Molecular and genetic studies of animal models have identified numerous genes that may cause or contribute to the development of obesity. They have also provided significant insight into the peripheral and central pathways that control energy intake and expenditure. Genetic studies of families and populations have generated useful information on genes and mutations associated with or linked to obesity, body fat distribution, and other relevant phenotypes. This information, combined with knowledge of the chromosomal location of genes identified from animal studies, has made it possible to identify specific mutations that contribute to the development of obesity in humans.

Adolescent↗
PubMed2000

Metabolic complications of obesity.

The rising prevalence of obesity is accompanied by an increasing number of patients with the metabolic complications of obesity. The major complications come under the heading of the metabolic syndrome. This syndrome is characterized by plasma lipid disorders (atherogenic dyslipidemia), raised blood pressure, elevated plasma glucose, and a prothrombotic state. The clinical consequences of the metabolic syndrome are coronary heart disease and stroke, type 2 diabetes and its complications, fatty liver, cholesterol gallstones, and possibly some forms of cancer. At the heart of the metabolic syndrome is insulin resistance, which represents a generalized derangement in metabolic processes. Obesity is the predominant factor leading to insulin resistance, although other factors play a role. The mechanistic link between insulin resistance and the metabolic syndrome is complex. The relationship is modulated by yet other factors, such as physical activity, body fat distribution, hormones, and a person's genetic polymorphic architecture. A better understanding of the molecular basis of this relationship is needed to suggest new targets for prevention and treatment of the complications of obesity. In addition, understanding at the clinical level will lead to improved management of these complications.

Blood Pressure↗
PubMed2005

Comparison of CT and dual-energy DEXA using a modified trunk compartment in the measurement of abdominal fat.

The quantification of abdominal fat is a marker of health risk. While dual-energy x-ray absorptiometry (DEXA) is easily applied, it measures overall fat, although abdominal fat may be a better indicator of health risk from obesity. We have evaluated whether a subcomponent of DEXA measurements correlates better with computed tomography (CT) for body fat than those traditionally used. Forty-seven healthy adults (22 M/25 F), aged 54.5+/-15.8 yr (mean+/-SD), with BMI of 27.1+/-4.6 kg/m2 participated in a cross-sectional study. Body fat was measured using abdominal CT and DEXA for total fat, trunk fat, and a modified trunk measurement that excludes the chest, termed "lower trunk," and compared. The coefficient of variation for DEXA measurements for trunk, lower trunk, and total body were 1.98, 3.12, and 0.85%, respectively. Mean DEXA for percentage fat ranged from 31.7% to 34.1% for trunk, lower trunk, and total body, compared to 54.2% for abdominal CT (p<0.003 for each pairwise comparison). Lower trunk, whole trunk, and total body DEXA measurements were not different. Measurement of subcomponents of fat content by DEXA is not superior to whole body measurements and remains consistently lower than measurements by CT.

Abdominal Fat↗