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Obesity is a major factor contributing to hypertension and increased risk of cardiovascular disease. Regular consumption of dietary fish and omega3 fatty acids of marine origin can lower blood pressure (BP) levels and reduce cardiovascular risk. This study examined the potential effects of combining dietary fish rich in omega3 fatty acids with a weight loss regimen in overweight hypertensive subjects, with ambulatory BP levels as the primary end point. Using a factorial design, 69 overweight medication-treated hypertensives were randomized to a daily fish meal (3.65 g omega3 fatty acids), weight reduction, the 2 regimens combined, or a control regimen for 16 weeks. Sixty-three subjects with a mean+/-SEM body mass index of 31.6+/-0.5 kg/m2 completed the study. Weight fell by 5.6+/-0.8 kg with energy restriction. Dietary fish and weight loss had significant independent and additive effects on 24-hour ambulatory BP. Effects were greatest on awake systolic and diastolic BP (P<0.01); relative to control, awake pressures fell 6.0/3.0 mm Hg with dietary fish alone, 5.5/2.2 mm Hg with weight reduction alone, and 13.0/9.3 mm Hg with fish and weight loss combined. These results also remained significant after further adjustment for changes in urinary sodium, potassium, or the sodium/potassium ratio, as well as dietary macronutrients. Dietary fish also significantly reduced 24-hour (-3.1+/-1.4 bpm, P=0.036) and awake (-4.2+/-1.6 bpm, P=0. 013) ambulatory heart rates. Weight reduction had a significant effect on sleeping heart rate only (-3.2+/-1.7 bpm, P=0.037). Combining a daily fish meal with a weight-reducing regimen led to additive effects on ambulatory BP and decreased heart rate. The effects were large, suggesting that cardiovascular risk and antihypertensive drug requirements are likely to be reduced substantially by combining dietary fish meals rich in omega3 fatty acids with weight-loss regimens in overweight medication-treated hypertensives. The reduction in heart rate seen with dietary fish suggests a cardiac/autonomic component, as well as vascular effects, of increased consumption of omega3 fatty acid from fish.
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PMID:Effects of dietary fish and weight reduction on ambulatory blood pressure in overweight hypertensives. 977 68

Because the biological and clinical significance of a genetic variant of luteinizing hormone (LH) is unclear, we therefore evaluated the occurrence of variant LH in women with a history of recurrent spontaneous abortion (RSA) and related it to specific LH concentrations, luteal function and pregnancy outcome. Of the 85 RSA women, 30 (35.3%) had variant LH (28 heterozygous and two homozygous), and 55 women (64.7%) a normal wild-type LH ratio. These frequencies are similar to those reported from the general Finnish population. No significant differences were observed in specific LH concentrations based on LH status (7.2+/-1.4 IU/l, mean +/- SEM, variant LH, versus 8.5+/-1.6 IU/l, wild-type LH). Variant LH was twice as common in women with body mass index (BMI) > 25 kg/m2 (9/15, 60.0%) than in those with BMI < or =25 kg/m2 (21/70, 30.0%, P < 0.05). The presence of variant LH was not associated with any clear effect on endocrine variables such as endometrial maturation or mid-luteal phase oestradiol and progesterone concentrations. During follow-up, 23 women with variant LH (76.7 %) and 41 with wild-type LH (74.5%) became pregnant: 14 miscarried (21.9%, six with variant LH and eight with wild-type LH) and two had ectopic pregnancies, whereas 48 (75.0%) succeeded (17 with variant LH and 31 with wild-type LH). LH concentrations before pregnancy were similar in women with a successful outcome (8.0+/-1.3 IU/l) or with a miscarriage also in that pregnancy (7.4+/-1.4 IU/l). In conclusion, variant LH is common in RSA women who are relatively overweight (BMI > 25 kg/m2) but its presence is not reflected in endometrial maturation and miscarriage rates.
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PMID:Genetic variant of luteinizing hormone in women with a history of recurrent miscarriage. 980 16

To determine the pathophysiological implications of serum leptin level in obesity, we monitored the changes in serum leptin level during outpatient treatment with life style modification in children. Fifty-five obese Japanese children (34 boys and 21 girls; mean age, 9.64 years) were studied. The control children consisted of 42 nonobese subjects (27 boys and 15 girls). The serum leptin concentration was 4.35 +/- 0.46 ng/ml (mean +/- SEM) in the control girls and 2.93 +/- 0.21 ng/ml in the control boys. The serum leptin concentrations in the obese boys and girls were higher than those in their lean counterparts. The concentration in the obese boys (16.28 +/- 1.41 ng/ml) was similar to that in the obese girls (20.33 +/- 2.0 ng/ml). The logarithmic value of serum leptin concentration at the first blood sampling in obese children was correlated with percent overweight and percent body fat. In 36 obese children (24 boys and 12 girls) whose serum leptin concentrations were monitored serially during treatment of obesity, the percent overweight was significantly decreased after the initial sampling. In each individual, the changes in leptin concentration were roughly parallel to those in percent overweight. The ratio of the leptin concentration at the second blood sampling divided by the one at the first sampling in each individual was closely correlated with the respective delta percent overweight. These results suggest that the preceding course of obesity determines the serum leptin level of obese children on longitudinal basis, and that the leptin level reflects the degree of obesity on cross-sectional basis.
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PMID:Changes in serum leptin concentration during behavioral therapy in obese children. 1067 Jul 57

While lifestyle modification decreases cardiovascular risk, there are barriers to lifestyle education in usual clinical practice, especially among the medically underserved. To address this gap, "Lighten Up," a church-based lifestyle program was developed in collaboration with the local African-American Christian community. Lighten Up includes a baseline health assessment (week 1), eight educational sessions (weeks 2-9) combining study of scripture and a health message, a short-term health check (week 10) and a long-term health check (week 52). Baseline and 10 week risk factor data have been obtained in 133 African Americans from eight sites (83% women) and form the basis of this report. At baseline, 76% of participants had two or more modifiable risk factors (overweight, hypertension, borderline high cholesterol, or diabetes). The entire group had significant short-term reductions in weight (-2.3 pounds, P<.01), mean blood pressure (BP, -2.1 mm Hg, P<.05), and triglycerides (-11 mg/dl, P<.05). Risk factor improvement was greater among the 60 subjects who attended 75% or more of the educational sessions. In this group, weight fell 2.9+/-0.6 pounds (mean +/- SEM; P<.01), mean BP declined 3.8+/-1.2 mm Hg (P<.01), total cholesterol was lowered 6+/-4 mg/ dl (P = .12), and triglycerides were reduced 17+/-9 mg/dl (P = .05). Lighten Up is reaching a group with multiple cardiovascular risk factors that is not optimally managed by existing healthcare resources. Of the 133 participants, 70% attended half or more of the sessions, and several components of the risk factor cluster were favorably affected.
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PMID:Short-term impact of a church-based approach to lifestyle change on cardiovascular risk in African Americans. 1076 26

Controversial effects of weight reduction on gonadotropin secretion in obesity have been reported. As a result of pulsatility, single serum samples or frequent sampling studies are somewhat limited with regard to monitoring LH and FSH concentrations. We studied follicular phase nocturnal urinary (nu) LH and FSH secretion and glucose metabolism (150-min euglycemic hyperinsulinemic clamp) during 1 menstrual cycle/30-day period before and after weight reduction in 10 severely overweight infertility patients (age, 29 +/- 3.1 yr; body mass index, 37.1 +/- 3.3 kg/m2; +/-SEM). A 6-week very low calorie diet was followed by a 4-week normocaloric period. The urinary LH and FSH results reported represent samples taken 12 to 2 days before the LH surge, or 10 consecutive samples in the case of amenorrhea. We observed a decrease of 8% (P < 0.001) in percent body fat mass and a 5% (P < 0.005) reduction in waist to hip ratio. Mean nu-LH decreased by 45% [6.06 +/- 1.05 (+/-SEM) to 3.22 +/- 0.71 IU/L], whereas mean nu-FSH remained unchanged. Insulin-stimulated glucose uptake increased by 41% (P < 0.01), which was accounted for by a significant increase in nonoxidative glucose disposal (P = 0.003). Serum sex hormone-binding globulin concentrations increased by 39% (P < 0.01), and insulin-like growth factor (IGF)-binding protein-1 (IGFBP-1) levels increased by 46% (P < 0.05). Fasting serum insulin concentrations decreased by 38%, those of leptin by 37%, those of androstenedione by 32%, those of testosterone by 20% (all P < 0.01), and those of dehydroepiandrosterone sulfate by 13% (P < 0.05). The percent change in nu-LH correlated negatively with glucose uptake (r = -0.76; P < 0.01) and the increase in serum sex hormone-binding globulin (r = -0.85; P < 0.005) and positively with the percent change in waist to hip ratio (r = 0.79; P < 0.01). The absolute nu-LH levels after weight reduction correlated significantly with fasting insulin concentrations (r = 0.88; P < 0.001) and negatively with glucose uptake (r = -0.67; P < 0.05). No significant relationships were found between absolute levels or changes in nu-LH concentrations and leptin, IGF-I, IGFBP-3, or IGFBP-1 concentrations. Our findings suggest that weight reduction with a very low calorie diet results in a decrease in nu-LH concentrations, a reduction in the LH/FSH ratio, and FSH predominance favoring folliculogenesis. The decrease in LH concentrations is inversely related to the severity of insulin resistance. It is possible that the decrease in LH secretion with weight reduction is more dependent on the absolute levels of insulin sensitivity than on the degree of general adiposity.
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PMID:The decrease in luteinizing hormone secretion in response to weight reduction is inversely related to the severity of insulin resistance in overweight women. 1099 21

Recent studies have suggested a short-term impairment in the regulation of food intake in older adults, but further studies are needed to determine if a longer-term impairment exists and to identify underlying causes. Changes in body weight and composition were measured over a 6-week underfeeding study and a 6-month follow-up period in healthy young (n = 23) and older (OLD, n = 18) men and women. The young adults were either normal weight (YNW, n = 12) or overweight (YOW, n = 11). Energy intakes during underfeeding were 896 +/- 18 (SEM) kcal less than weight-maintenance energy requirements determined prior to underfeeding. In addition, changes in perceived hunger during underfeeding were monitored in a subgroup (n = 19). OLD and YOW subjects lost significantly more weight during underfeeding than did YNW subjects (p = .025 and .000, respectively), and they did not gain back significant weight in the 6-month follow-up. In addition, OLD subjects reported a significantly lower frequency of hunger during underfeeding (p = .05). There was no significant difference among groups in the relationship between weight lost and fat-free mass lost. Healthy OLD adults have an impaired ability to regulate food intake over at least 6 months following underfeeding compared with YNW adults, and a reduction in their perceived frequency of hunger may be a contributing factor.
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PMID:Effects of a 6-week hypocaloric diet on changes in body composition, hunger, and subsequent weight regain in healthy young and older adults. 1112 87

Hormonal abnormalities of the reproductive axis have been described in obesity. In men, extreme obesity is associated with low serum testosterone (T) and high estrogen [estrone and estradiol (E(2))] levels. As changes in the sex steroid milieu may profoundly affect the carbohydrate heterogeneity and thus some of the biological and physicochemical properties of the LH molecule, we analyzed the relative distribution of LH isoforms circulating under baseline conditions (endogenous GnRH drive) as well as the forms discharged by exogenous GnRH stimulation from putative acutely releasable and reserve pituitary pools in overweight men. Secondarily, we determined the impact of the changes in LH terminal glycosylation on the in vitro bioactivity and endogenous half-life of the gonadotropin. Seven obese subjects with body mass indexes ranging from 35.7-45.5 kg/m(2) and seven normal men with body mass indexes from 22.5-24.2 kg/m(2) underwent blood sampling at 10-min intervals for a total of 10 h before and after the iv administration of 10 and 90 microg GnRH. Basally released and exogenous GnRH-stimulated serum LH isoforms were separated by preparative chromatofocusing and identified by RIA of eluent fractions. Serum pools of successive samples collected across 2-h intervals (five serum pools per subject) containing LH released under baseline and exogenous GnRH-stimulated conditions were tested for bioactivity employing a homologous in vitro bioassay. Mean serum T and E(2) levels were significantly lower and higher, respectively, in the obese men than in the control group [serum T, 13.5 +/- 2.4 vs. 19.4 +/- 1.4 nmol/L (mean +/- SEM; P: = 0.01); serum E(2), 0.184 +/- 0.01 vs. 0.153 +/- 0.01 nmol/L (P: < 0.05)]. Mean baseline serum LH levels were similar in obese subjects and normal controls (13.3 +/- 1.3 and 12.2 +/- 1.2 IU/L). Although multiple parameter deconvolution of the exogenous GnRH-induced LH pulses revealed that the magnitude of the pituitary response in terms of secretory burst mass, secretory amplitude, and half-duration of the LH pulses was similar in obese and control subjects, the apparent endogenous half-life of LH was significantly (P: < 0.05) shorter in the obese group (98 +/- 11 min) than in the normal controls (132 +/- 10 min). Under all conditions studied, the relative abundance of basic isoforms (those with pH >/=7.0) was significantly (P: < 0.05) increased in the obese subjects compared with the controls (percentages of LH immunoactivity recovered at pH >/=7.0: obese subjects, 34-57%; normal controls, 22-46%). The biological to immunological ratio of LH released in baseline and low dose (10 microg) GnRH-stimulated conditions were similar in obese subjects and normal controls, whereas LH released by obese subjects in response to the high (90 microg) GnRH dose exhibited significantly lower ratios than those detected in normal individuals (0.62 +/- 0.07 and 0.45 +/- 0.09 vs. 1.01 +/- 0.10 and 0.81 +/- 0.09 for LH released within 10-120 min and 130-240 min after GnRH administration in obese and controls, respectively; P: < 0.05). Collectively, these results indicate that the altered sex steroid hormone milieu characteristic of extreme obesity provokes a selective increase in the release of less acidic LH isoforms, which may potentially modify the intensity and duration of the blood LH signal delivered to the gonad. Altered glycosylation of LH may therefore represent an additional mechanism modulating the hypogonadal state prevailing in morbid obesity.
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PMID:A preponderance of circulating basic isoforms is associated with decreased plasma half-life and biological to immunological ratio of gonadotropin-releasing hormone-releasable luteinizing hormone in obese men. 1113 15

Subjects with impaired glucose tolerance (IGT) are usually overweight and exhibit insulin resistance with a defective compensation of insulin secretion. In this study, we sought to establish the interrelation between insulin secretion and insulin sensitivity after oral glucose in non-obese subjects with IGT and we also examined this interrelation in relation to the 2 main incretins, glucagon-like peptide (GLP-1) and gastric inhibitory polypeptide (GIP). To that end, 13 women with IGT and 17 women with normal glucose tolerance (NGT) underwent an oral glucose tolerance test (OGTT) with measurements of glucose, insulin, C-peptide, GLP-1, and GIP. Insulin secretion (TIS) and insulin sensitivity (OGIS) were assessed using models describing the relationship between glucose, insulin and C-peptide data. These models allowed estimation also of the hepatic extraction of insulin. The age (54.2 +/- 9.7 [mean +/- SD] years) and body mass index (BMI; 26.0 +/- 4.0 kg/m(2)) did not differ between the groups. Subjects with IGT displayed lower TIS during the initial 30 minutes after oral glucose (0.97 +/- 0.17 [mean +/- SEM] v 1.75 +/- 0.23 nmol/L in NGT; P =.018) and lower OGIS (397 +/- 21 v 463 +/- 12 mL/min/m(2); P =.005). The incremental 30-minute TIS times OGIS (reflecting insulin secretion in relation to insulin sensitivity) was significantly reduced in IGT (359 +/- 51 v 774 +/- 91 nmol/min/m(2), P =.001). This measure correlated inversely to the 2-hour glucose level (r = -0.71; P <.001). In contrast, TIS over the whole 180-minute period was higher in IGT (26.2 +/- 2.4 v 20.0 +/- 2.0 nmol/L; P =.035). Hepatic insulin extraction correlated linearly with OGIS (r = 0.71; P <.001), but was not significantly different between the groups although there was a trend with lower extraction in IGT (P =.055). Plasma levels of GLP-1 and GIP increased after oral glucose. Total secretion of these incretin hormones during the 3-hour test did not differ between the 2 groups. However, the 30-minute increase in GLP-1 concentrations was lower in IGT than in NGT (P =.036). We conclude that also in non-obese subjects with IGT, when adiposity is controlled for in relation to NGT, defective early insulin secretion after oral glucose is a key factor. This defective beta-cell function is associated with, and may be caused by, a reduced early GLP-1 response.
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PMID:Insulin secretion and incretin hormones after oral glucose in non-obese subjects with impaired glucose tolerance. 1513 68

Obesity is a risk factor for arterial hypertension. We studied the relationships between the body mass index (BMI) and the nycthemeral pattern of blood pressure (BP), renal function and sodium and water excretion (EX) in a group of 25 moderately hypertensive untreated men (41 +/- 2 y, 80 +/- 3 kg). Subjects were given a high sodium diet (6 g NaCl added to their usual diet, daily EX=200 mmol). On the 7th day, BP was monitored during 24 h and urine collected in 2 fractions (day=D, 8:00-22:00 and night=N, 22:00-8:00). Subjects were a posteriori divided into 2 groups according to the median BMI (26 kg/m2): Group 1, n=12, BMI 23.2 +/- 0.6 (mean +/- SEM) and Group 2, n=13, BMI 29.2 +/- 0.5 kg/m2. No difference was observed between the two groups for age, 24 h urine and sodium EX, or systolic and diastolic BP. However, heart rate was significantly higher during N in Group 2 (66 +/- 2 vs 57 +/- 2 b/min, p=0.012). Na and water EX were significantly higher during D than during N in Group 1, but lower during D than during N in Group 2. Creatinine clearance was higher in Group 2 than in Group 1 especially during N (D+29%, p=0.013; N+49%, p<0.001). In Group 2, subjects concentrated their urine more than in Group 1, as evaluated from the urine/plasma creatinine ratio (+49%, p=0.019). This ratio was positively correlated to BMI during D (r=0.561, p=0.004) but not during N. These results show that the glomerular hyperfiltration associated with overweight is more intense at night and that moderately overweight hypertensives have a reduced sodium and water EX during the day and a compensatory larger EX at night. The reduced diurnal EX goes along with an increased urine concentration. The nocturnal rise in EX is concomittant with a rise in heart rate. Given the growing health problems linked to obesity and hypertension, these results open a new field for the understanding of the difficulty to excrete sodium in this condition.
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PMID:[Influence of moderate body weight excess on the nycthemeral pattern of blood pressure, renal function and sodium and water excretion in patients with essential hypertension]. 1550 65

Epidemiological studies have reported that women with osteoporosis present an increased risk of cardiovascular events and that lipid lowering therapy (statins) could be associated with a decreased risk of fracture. We investigated whether women with atherogenic lipid profile have lower lumbar and femoral bone mineral density (BMD) and higher prevalence of osteopenia than those with normal lipid levels. The study included 52 overweight early postmenopausal women, with no history of hormone replacement therapy, or any current or past pathology or treatment that could alter bone or lipid metabolism. Atherogenic lipid profile or hyperlipidemia was defined as hypercholesterolemia (> or = 240 mg/dl) or high low-density lipoprotein cholesterol (high-LDLc > or = 160 mg/dl) or high lipoprotein (a) [high-Lp (a) > or =25 mg/dl], and low-BMD as t-score <-1 SD at lumbar o femoral site. The results show that women with hyperlipidemia had lower mean-adjusted BMD (mean+/-SEM) at lumbar (0.865+/-0.020 vs. 0.958+/-0.028 g/cm2, p = 0.007) and femoral neck (0.712+/-0.015 vs. 0.796+/-0.021, p = 0.004 g/cm2) than those with normal lipid levels. Hypercholesterolemia group had higher prevalence of low-BMD at lumbar spine (82.6% vs. 55.2%, p = 0.04, OR: 3.8; 95% CI: 1.04-14.2) and femoral neck (65.2% vs. 37.9%, p = 0.05, OR: 3.1; 95% CI: 0.98-9.6). The high-LDLc group had also higher prevalence low-BMD at femoral neck (75% vs. 39%, p = 0.01, OR: 4.7; 95% CI: 1.26-17.5), and the high-Lp (a) group at lumbar spine (87% vs. 51.7% p = 0.007, OR: 6.2; 95% CI: 1.5-25.6). Women with hyperlipidemia had higher prevalence of low BMD at lumbar spine (81.8% vs. 42.1%, p = 0.003, OR: 6.2; 95% CI: 1.7-22) and femoral neck (60.6% vs. 31.6%, p = 0.04, OR: 3.3; 95% CI: 1.01-11.0). In conclusion, early postmenopausal women with atherogenic lipid profile, defined as cholesterol > or =240 mg/dl or LDLc > or = 160 mg/dl or Lp(a) > or = 25 mg/dl have lower lumbar and femoral BMD and have an increased risk of osteopenia than those with normal lipid profile, suggesting that hyperlipidemia could be associated with osteoporosis and bone status should be evaluated in women with hyperlipidemia.
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PMID:Atherogenic lipid profile and elevated lipoprotein (a) are associated with lower bone mineral density in early postmenopausal overweight women. 1567 90


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