Serum Leptin and Weight Gain Over 8 Years in African American and Caucasian Young Adults

FOLSOM, AARON R., MICHAEL D. JENSEN, DAVID R. JACOBS, JR., JOAN E. HILNER, ALBERT W. TSAI, AND PAMELA J. SCHREINER. Serum leptin and weight gain over 8 years in African American and Caucasian young adults. Obes Res. 1999;7:1–8. Objective : There is considerable interest in how to prevent weight gain in adulthood. Leptin, a peptide hormone expressed in adipose tissue, is believed to signal the central nervous system about the level of body fat stores, and thereby may control appetite. Little information exists on whether the serum leptin concentration influences long-term weight changes in the free-living population. Research Methods and Procedures : From an ongoing cohort study of young African American and white adults, we selected a sample of participants (n=492), stratified on sex, race, and weight changes over 8 years. Serum leptin was measured on stored specimens using a radioimmunoassay. Weight change was modeled in relation to baseline leptin concentrations. Results : Cross-sectionally, leptin concentration was associated positively with body mass index, negatively with physical activity level, and was higher in women than men. These variables explained 72% of the variance in serum leptin. Over the 8 years, the sample gained an average of 7.8 kg (standard deviation = 10.8). There was no evidence that 8-year weight change was associated with initial leptin concentration: 8-year weight change was only 0.5 kg less (95% confidence interval = ?1.8 to 0.8, p = 0.47) per each 10 ng/ mL increment (approximately one standard deviation) of baseline leptin. In contrast, leptin change correlated highly (r = 0.62) with weight change. Discussion : Our data corroborate evidence that adiposity determines leptin levels but do not support the hypothesis that leptin deficiency plays an important role in obesity in the general population.     

A Prospective Study of the Effect of Childbearing on Weight Gain in African‐American Women

Objective: To prospectively assess the influence of bearing a first, second, or later child on weight gain among African‐American women in the context of other risk factors. Research Methods and Procedures: Data were obtained in a prospective follow‐up study of African‐American women from across the U.S. who are participants in the Black Women's Health Study. Postal questionnaires were used to collect baseline data in 1995 and follow‐up data in 1997 and 1999. Parous and nulliparous women (11, 196) (21 to 39 years old at baseline), of whom 1230 had a singleton birth during follow‐up, are the subjects of the present analyses. We assessed change in BMI (kilograms per meter squared) in relation to childbearing during 4 years of follow‐up, with use of multivariable linear regression to control for important risk factors. Results: During 4 years of follow‐up, the BMI of participants increased by an average of 1.6 kg/m², equivalent to a weight gain of ～4.4 kg. Women who had a child during follow‐up gained more weight than women who remained nulliparous, and those who had a first child gained more than those who had a second or later child. The weight gain associated with childbearing increased with increasing baseline BMI and was appreciable among heavier women. For example, among women with a baseline index of 36, the increase in BMI for women who bore a first child was 1.1 kg/m² more than that of nulliparous women, equivalent to a difference in weight gain of ～3.0 kg. Discussion: Childbearing is an important contributor to weight gain among African‐American women.     

Serum Leptin Concentrations and Weight Gain in Postobese,Postmenopausal Women

Objective : This study was designed to determine if serum leptin concentrations (adjusted for fat mass) after weight loss on a low-calorie diet predict subsequent weight gain. Research Methods and Procedures : Body composition and serum leptin concentrations were determined on 14 moderately obese, postmenopausal, nondiabetic women with a familial predisposition to obesity. Assessments were obtained under tightly controlled metabolic ward conditions of macronutrient intake and weight maintenance both before (obese state) and after a mean weight loss of 12.0 kg to normal body weight (postobese state). Four years later, without intervention, body weight and body composition were reassessed. Results : Weight loss resulted in significant decreases in fat mass (29.7 ± 5.4 vs. 20.3 ± 4.7; kg), body mass index (27.7 ± 1.6 vs. 23.0 ± 1.5; kg/m2), percent body fat (40.7 ± 4.3 vs. 33.1 ± 5.0), and serum leptin concentrations (31.8 ± 16.0 vs. 11.5 ± 5.4; ng/mL). Serum leptin concentrations were positively correlated (p<<0.05) with fat mass in both the obese and postobese states (r = 0.67 and r = 0.56, respectively). However, residual serum leptin concentrations (adjusted for fat mass) in the obese and postobese states were not related to changes in body weight (p<= 0.61 and 0.52), fat mass (p = 0.72 and 0.42), body mass index (p = 0.59 and 0.33), or percent body fat (p = 0.84 and 0.46) over the follow-up period. Discussion : These finding do not support the hypothesis that relatively low concentrations of leptin predict weight regain after weight loss. However, because the number of subjects in this study was limited, further studies are warranted.     

Lean and Weight Stable: Behavioral Predictors and Psychological Correlates

Objective: To examine behavioral characteristics associated with being lean and weight stable during adulthood. Research Methods and Procedures: Participants included 165 white married couples who were part of a larger longitudinal study. Participants’ height and weight were measured on three occasions at 2‐year intervals. Men and women were classified as being lean and weight stable (the target group) if they had a BMI < 25 at baseline and maintained their weight within 5% of baseline at 2nd and 4th year follow‐up. Individuals not fulfilling these criteria were included in the comparison group. Group differences in background characteristics including childhood weight status, BMI at each occasion, dieting history, and mental and physical health history were examined. In addition, multiple measures of dietary intake and physical activity were obtained and used to predict the likelihood of being in the target group. Results: Men (N = 22) and women (N = 36) in the target group had lower mean BMI scores at each occasion, were less overweight during childhood, were less likely to have dieted in the past year, and rated themselves as being more healthy than men and women in the comparison group. No differences were identified in mental health. Relative to the comparison group, women in the target group reported higher levels of physical activity and higher levels of physical activity among their spouses, and men in the target group reported healthier dietary patterns. Discussion: Results from this study suggest that being lean and weight stable in adulthood is linked to childhood weight status in combination with dietary and activity patterns during adulthood.     

Gender Differences in the Response of Plasma Leptin Concentrations to Weight Loss in Obese Older Individuals

Plasma leptin concentration is directly related to the degree of obesity and is higher in women than in men of the same body mass index (BMI). We hypothesized that fasting plasma leptin concentrations and the response of leptin to weight loss would differ in older men and women of a similar fat mass. Plasma leptin concentrations (radioimmunoassay) and fat mass (DXA) were measured in 47 older, obese (BMI=30 ± 4 kg/m²) women and 23 older, obese (BMI=31 ± 3 kg/m²) men after a 2 to 4 week period of weight and dietary stabilization, and then in 22 of the women and 18 of the men after a 6-month weight loss intervention (250–350 kcal/d deficit). Leptin correlated with fat mass in men and women (r=0.75 and r=0.77, respectively; p values<0.0001), but women had 3-fold higher leptin levels for a given fat mass than men (p=0.01). In response to the 6-month hypocaloric diet, men and women lost a similar percentage of fat mass (?13% and ?16%, respectively), but the relative decline in circulating leptin was greater in women than men (-45% and ?21%, respectively; p<0.0001). In addition, when leptin was normalized for fat mass using the ratio method, the decrease in leptin per kilogram of fat mass was greater in women than men (-0.37 ± 0.34 vs. ?0.04 ± 0.06 ng/mL/kg; p<0.01). After weight loss, the change in leptin concentrations correlated positively with the change in fat mass in men (r=0.60; p<0.01), but not in women (r=0.31; p=0.17). Furthermore, the loss in fat mass correlated negatively with baseline leptin levels in women (r=-0.47; p<0.05), but not in men (r=0.03, p=NS). These results indicate that the decline in leptin concentration with weight loss correlates with the loss in fat mass in men; but, in women, other factors affect the decrease in leptin concentration. This suggests that the role of leptin in the regulation of obesity is gender-specific and may account for gender differences in response to hypocaloric treatment and maintenance of lost weight.     

Weight cycling and 6-year weight change in healthy adults: The Aerobics Center Longitudinal Study

Objective: To determine the longitudinal relationship between a reported history of weight cycling and the trajectory of weight in a group of normal‐weight to obese women and men. Research Methods and Procedures: This was a clinic‐based cohort study conducted over 6 years. Subjects were healthy women (n = 141) and men (n = 797) age 20 to 78 years who completed at least four comprehensive medical exams at the Cooper Clinic (Dallas, TX) between 1987 and 2003. Weight loss history was reported, and body weight was measured at all examinations. Weight cycling status was derived from weight loss history and defined as ≥five episodes of weight loss of ≥2.3 kg/episode. Using linear mixed effects models, weight at each examination was regressed on weight cycling status separately for women and men while controlling for selected covariables. Results: Baseline BMI was 23 and 21 kg/m² among cycling and non‐cycling women and was 27 and 25 kg/m² among cycling and non‐cycling men, respectively. We observed a non‐significant difference (p = 0.09) in women by cycling status (average weight gain = 0.5 and 0.2 kg/yr among cyclers and non‐cyclers, respectively) and no difference in weight gain over time among men by cycling status (average weight gain = 0.2 kg/yr among both groups, p = 0.99). Higher baseline cardiorespiratory fitness level and increased fitness over the follow‐up were associated with attenuated weight gain in both women and men. Discussion: In healthy, middle‐aged individuals, a history of weight cycling does not seem to increase the risk of long‐term weight gain in men; however, this relation needs to be studied further in women.     

Genetic Variation in the Leptin Receptor Gene,Leptin, and Weight Gain in Young Dutch Adults

Objective: To investigate the association between leptin levels, polymorphisms in the leptin receptor (LEPR) gene, and weight gain. Research Methods and Procedures: From two large prospective cohorts in The Netherlands (n = 17, 500), we compared the baseline leptin of 259 subjects who had gained an average of 12.6 kg (range 5.5 to 33 kg) with 277 subjects who kept stable weight (range ?2.6 to 3.1 kg) after a mean follow‐up of 6.8 years. Three polymorphisms in the LEPR gene (Lys109Arg, Gln223Arg, and Lys656Asn) were determined. Results: Weight gainers had significantly higher baseline leptin levels than those who kept stable weight (odds ratio = 1.27, 95% confidence interval 1.1 to 1.5, per SD increase in log_e‐transformed leptin). Weight gainers with the Arg109 or the Arg223 alleles had higher leptin levels compared with the noncarriers of these alleles. Only among men, the association between leptin and weight gain tended to be stronger among those with an Arg223 allele compared with those without this mutation. Discussion: Relatively high leptin levels predict weight gain, suggesting that leptin resistance plays a role in the development of obesity in the general population. Higher leptin levels for those with a Lys109Arg or Gln223Arg mutation (or a linked other marker) may imply that these subjects have a modified functional leptin receptor. However, the role of these mutations on weight gain is limited.     

Birth Weight,Adult Body Composition,and Subcutaneous Fat Distribution

Objectives: To investigate if birth weight is related to both body mass index (BMI) and distribution of subcutaneous fat at adult age. Research Methods and Procedures: A 9‐year longitudinal study was performed in 229 subjects (192 women) with ages ranging from 27 to 36 years. Birth weight was retrieved by a questionnaire, and adult weight, height, skinfold thicknesses, and waist‐to‐hip ratio (WHR) were repeatedly measured at mean ages 27, 29, 31, and 36 years. BMI, sum of four skinfolds (S4S), the ratio between two truncal skinfolds and S4S (SS/S4S), and the ratio between WHR and the cross‐sectional area of the left thigh were calculated with the available data. Results: The adjusted model showed that in women, birth weight was significantly negatively related to adult S4S [β = ?5.211; (?9.768 to ?0.654)], waist circumference [β = ?1.449; (?2.829 to ?0.069)], and SS/S4S ratio [β = ?3.579; (?5.296 to ?1.862)]. In men, a significant negative association was observed between birth weight and adult WHR [β = ?1.096; (?2.092 to ?0.100)] only. Other relationships showed, although not significantly, the same negative trend, namely that lower birth weight is related to higher adult body fat mass (S4S) and a more truncal subcutaneous fat distribution (SS/S4S). No associations were found between birth weight and either adult BMI or the cross‐sectional area of the thigh. Discussion: Lower birth weight is, in both adult men and women, related to a higher adult subcutaneous fat mass and a more truncal distribution of subcutaneous fat, indicating a higher risk for obesity.     

Weight gain prevention among women

Objective: Women 25 to 45 years old are at risk for weight gain and future obesity. This trial was designed to evaluate the efficacy of two interventions relative to a control group in preventing weight gain among normal or overweight women and to identify demographic, behavioral, and psychosocial factors related to weight gain prevention. Research Methods and Procedures: Healthy women (N = 284), ages 25 to 44, with BMI < 30 were randomized to one of three intervention conditions: a clinic‐based group, a correspondence course, or an information‐only control. Intervention was provided over 2 years, with a follow‐up at Year 3. BMI and factors related to eating and weight were assessed yearly. Results: Over the 3‐year study period, 40% (n = 114) of the women remained at or below baseline body weight (±2 lbs), and 60% gained weight (>2 lbs). Intervention had no effect on weight over time. Independently of intervention, women who were older, not actively dieting to lose weight, and who reported less perceived hunger at baseline were more likely to be successful at weight maintenance. Weight maintenance also was associated with increasing dietary restraint (conscious thoughts and purposeful behaviors to control calorie intake) and decreasing dietary disinhibition (the tendency to lose control over eating) over time. Discussion: This study raises concern about the feasibility and efficacy of weight gain prevention interventions because most women were interested in weight loss, rather than weight gain prevention, and the interventions had no effect on weight stability. Novel approaches to the prevention of weight gain are needed.     

Weight Change in Adult Life and Health Outcomes

Objective: To investigate the relationship between weight change in adult life and subsequent mortality and cancer incidence in women. Research Methods and Procedures: In 1994 to 1995, all women (age range, 42 to 81) still under general practitioner observation in the United Kingdom's Royal College of General Practitioners Oral Contraception Study (n = 12 303) were sent a health survey asking about health and lifestyle issues, including current weight and weight at age 30. The main outcome measures were 6‐year all‐cause mortality and cancer incidence among different weight change deciles. Cox regression was used to calculate hazard ratios that were adjusted for: social class at recruitment, BMI at age 30, and age group, parity, smoking status, and hormone replacement therapy status in 1995. Results: Women who had been obese at age 30 were more likely to die and significantly more likely to develop cancer in the 6 years after the health survey than non‐obese respondents. Women reporting weight gains between age 30 and 1995 were significantly less likely to die during the 6 years after the health survey than those with a stable weight, whereas those with weight loss did not fare any better than those in the stable‐weight group. Discussion: Although obesity at young age was associated with subsequent mortality and cancer incidence, weight gain over a time period of 12 to 51 years appeared to be beneficial when compared with women with stable weight over the same time period. Further research is needed to confirm or refute our findings and to allow detailed examination of potential explanations for them.     

A physiological role of breast milk leptin in body weight control in developing infants

Objective: Leptin, a hormone that regulates food intake and energy metabolism, is present in breast milk. The aim of this study was to determine whether milk leptin concentration is correlated with maternal circulating leptin and BMI and with body weight gain of infants. Research Methods and Procedures: A group of 28 non‐obese women (BMI between 16.3 and 27.3 kg/m²) who breast‐fed their infants for at least 6 months and their infants were studied. Venous blood and milk samples were obtained from mothers at 1, 3, 6, and 9 months of lactation, and leptin concentration was determined. Infant body weight and height were followed until 2 years of age. Results: During the whole lactation period, milk leptin concentration correlated positively with maternal plasma leptin concentration and with maternal BMI. In addition, milk leptin concentration at 1 month of lactation was negatively correlated with infant BMI at 18 and 24 months of age. A better negative correlation was also found between log milk leptin concentration at 1 and at 3 months of lactation and infant BMI from 12 to 24 months of age. Discussion: We concluded that, in a group of non‐obese mothers, infant body weight during the first 2 years may be influenced by milk leptin concentration during the first stages of lactation. Thus, moderate milk‐borne maternal leptin appears to provide moderate protection to infants from an excess of weight gain. These results seem to point out that milk leptin is an important factor that could explain, at least partially, the major risk of obesity of formula‐fed infants with respect to breast‐fed infants.     

Pre-Pregnancy Body Mass Index,Gestational Weight Gain,and Birth Weight: A Cohort Study in China

Objective

To assess whether pre-pregnancy body mass index (BMI) modify the relationship between gestational weight gain (GWG) and child birth weight (specifically, presence or absence of low birth weight (LBW) or presence of absence of macrosomia), and estimates of the relative risk of macrosomia and LBW based on pre-pregnancy BMI were controlled in Wuhan, China.

Methods

From June 30, 2011 to June 30, 2013. All data was collected and available from the perinatal health care system. Logistic regression models were used to estimate the independent association among pregnancy weight gain, LBW, normal birth weight, and macrosomia within different pre-pregnancy BMI groups. We built different logistic models for the 2009 Institute of Medicine (IOM) Guidelines and Chinese-recommended GWG which was made from this sample. The Chinese-recommended GWG was derived from the quartile values (25th-75th percentiles) of weight gain at the time of delivery in the subjects which comprised our sample.

Results

For LBW children, using the recommended weight gain of the IOM and Chinese women as a reference, the OR for a pregnancy weight gain below recommendations resulted in a positive relationship for lean and normal weight women, but not for overweight and obese women. For macrosomia, considering the IOM’s recommended weight gain as a reference, the OR magnitude for pregnancy weight gain above recommendations resulted in a positive correlation for all women. The OR for a pregnancy weight gain below recommendations resulted in a negative relationship for normal BMI and lean women, but not for overweight and obese women based on the IOM recommendations, significant based on the recommended pregnancy weight gain for Chinese women. Of normal weight children, 56.6% were above the GWG based on IOM recommendations, but 26.97% of normal weight children were above the GWG based on Chinese recommendations.

Conclusions

A GWG above IOM recommendations might not be helpful for Chinese women. We need unified criteria to classify adult BMI and to expand the sample size to improve representation and to elucidate the relationship between GWG and related outcomes for developing a Chinese GWG recommendation.     

Correlation between birth weight, leptin, zinc and copper levels in maternal and cord blood

Leptin and zinc are involved in the regulation of appetite. Copper is a trace element regulating the functions of several cuproenzymes that are essential for life. To evaluate the relationship between zinc and copper status and the leptin system in humans, we examined whether leptin concentrations in the mother and the newborn correlate with the weight of mother, placenta and newborn. A total of 88 pregnant women at 38-42 weeks' gestation were studied. All infants were categorized as small for gestational age (SGA) (n = 16), average for gestational age (AGA) (n = 59) or large for gestational age (LGA) (n = 13). Leptin, zinc, and copper levels were measured in maternal and cord serum at birth. Maternal BMI and placental weight of the LGA groups were significantly higher than those of the SGA and AGA groups. Cord and maternal leptin levels of the SGA groups were significantly lower than those of the AGA and LGA groups. Maternal serum leptin levels were positively correlated with BMI and maternal zinc levels in all groups. Cord serum leptin levels of all groups were positively correlated with birth weight and placental weight. Birth weight was negatively correlated with maternal and cord copper level of all groups. Umbilical leptin concentrations of SGA newborns correlated with leptin concentrations of their mothers. In all pregnancies, birth weight increases in association with increase in cord leptin level. Our results suggest that maternal zinc but not copper level has an effect on maternal serum leptin levels. The increase in copper level in both maternal and cord blood may contribute to restriction in fetal growth.     

Leptin Responses to Weight Loss in Postmenopausal Women: Relationship to Sex‐Hormone Binding Globulin and Visceral Obesity

Objective: Leptin concentrations increase with obesity and tend to decrease with weight loss. However, there is large variation in the response of serum leptin levels to decreases in body weight. This study examines which endocrine and body composition factors are related to changes in leptin concentrations following weight loss in obese, postmenopausal women. Research Methods and Procedures: Body composition (DXA), visceral obesity (computed tomography), leptin, cortisol, insulin, and sex hormone‐binding globulin (SHBG) concentrations were measured in 54 obese (body mass index [BMI] = 32.0 ± 4.5 kg/m²; mean ± SD), women (60 ± 6 years) before and after a 6‐month hypocaloric diet (250 to 350 kcal/day deficit). Results: Body weight decreased by 5.8 ± 3.4 kg (7.1%) and leptin levels decreased by 6.6 ± 11.9 ng/mL (14.5%) after the 6‐month treatment. Insulin levels decreased 10% (p < 0.05), but mean SHBG and cortisol levels did not change significantly. Relative changes in leptin with weight loss correlated positively with relative changes in body weight (r = 0.50, p < 0.0001), fat mass (r = 0.38, p < 0.01), subcutaneous fat area (r = 0.52, p < 0.0001), and with baseline values of SHBG (r = 0.38, p < 0.01) and baseline intra‐abdominal fat area (r = ?0.27, p < 0.06). Stepwise multiple regression analysis showed that baseline SHBG levels (r² = 0.24, p < 0.01), relative changes in body weight (cumulative r² = 0.40, p < 0.05), and baseline intra‐abdominal fat area (cumulative r² = 0.48, p < 0.05) were the only independent predictors of the relative change in leptin, accounting for 48% of the variance. Discussion: These results suggest that obese, postmenopausal women with a lower initial SHBG and more visceral obesity have a greater decrease in leptin with weight loss, independent of the amount of weight lost.     

Weight Loss and Leptin Changes in Individuals with Type 2 Diabetes

WILLIAMS, KATHERINE V., MONICA MULLEN, WE1 LANG, ROBERT V. CONSIDINE, AND RENA R. WING. Weight loss and leptin changes in individuals with type 2 diabetes. Obes Res. Objective To identify variables associated with leptin change in subjects with type 2 diabetes after 3 weeks and 20 weeks of weight loss. Research Methods and Procedures Subjects with type 2 diabetes treated with diet or sulfonylureas (n = 54) were enrolled in a 20-week behavioral weight control program. Sulfonylureas were stopped ≥2 weeks before study entry. Seven subjects who restarted sulfonylureas after week 3 had their data analyzed separately after this point. Results Leptin, fasting plasma glucose, and insulin levels were measured at baseline and at 3, 10, and 20 weeks. After 3 weeks, subjects lost 2.7±2.0 kg (p<0.001), and had significant decreases in leptin (5.2±7.0 ng/mL, p<0.001), fasting plasma glucose (1.8±1.8 mmol/L, p<0.001), and insulin (23±60 pmol/L, p<0.03). Between week 3 and week 20, subjects lost an additional 6.3±4.4 kg (P<0.001), but had no further changes in leptin. The primary determinants of leptin change at all time-points were weight loss and initial leptin level. Changes in insulin were not related to changes in leptin after controlling for the effects of weight loss. At week 20, more recent weight loss (week 10 to week 20) was as strong a predictor of overall change in leptin as overall weight loss (baseline to 20 week). Subjects who restarted sulfonylureas had an increase in both leptin levels (+1.9±9.0 ng/mL, p<0.05) and insulin levels (+23±65 pmol/L, p<0.05), despite significant overall weight loss (-7.4±4.0 kg, p<0.01). Initial changes in leptin (0 weeks to 3 weeks) did not affect subsequent ability to lose weight. Discussion Both short- and long-term changes in weight had an effect on leptin changes in individuals with type 2 diabetes. Although physiological insulin changes did not independently influence changes in leptin concentration with weight loss, increases in insulin levels with sulfonyl-urea therapy were associated with increases in leptin levels despite weight loss.     

Pregnancy Weight Retention in Morbid Obesity

HUNT, STEVEN C, MARIA M DAINES, TED D ADAMS, EDWARD M HEATH AND ROGER R WILLIAMS. Pregnancy weight retention in morbid obesity. Obes Res. 1995;3:121–130. Recent hypotheses suggest that for women who develop morbid obesity, increases in weight associated with pregnancy may represent a significant contribution to their obesity status. The effects of multiple pregnancies on weight gain were studied in 96 morbidly obese women (<13.6 kg over ideal weight at ages 20–24 or before an earlier first pregnancy and currently >44.5 kg over ideal weight) and 115 random control women from the Utah population. Self-reported weights for each pregnancy included: prepregnancy, greatest during pregnancy, and 6 weeks following delivery, which were validated against available hospital records. Mean number of pregnancies in each group were similar (4.2 and 4.3), ranging from 1 to 9. Mean current age was 46 and mean weight gain since ages 20–24 was 46.0 kg in the morbidly obese and 14.1 kg in controls. Regression of current weight on total number of pregnancies, adjusting for weight at ages 20–24, showed a 1.3 kg/pregnancy increase in current weight (p=0.03) with no difference between groups (p=0.6). Weight gain subsequent to the last pregnancy was not related to the number of pregnancies (p=0.2). Morbidly obese women gained more weight during pregnancy than controls only for the first pregnancy. Gains were similar for all other pregnancies. Morbidly obese women had smaller weight losses after delivery than the controls, but these differences were not significant. For the first pregnancy, morbidly obese women had a net weight retention that was 4.0 kg greater than the controls at 6 weeks post-partum and an average of 1.6 kg/pregnancy greater retention for the remaining pregnancies. Pregnancy weight gains for each pregnancy subsequent to the first pregnancy were constant. These findings suggest: 1) women who develop morbid obesity have slightly less weight loss after delivery and greater between-pregnancy weight gains than controls; 2) the number of pregnancies does not affect the amount of weight gained after the last pregnancy; and 3) while multiparity may augment weight gain in morbidly obese women, it is probably not a primary factor in the later development of morbid obesity.     

Effect of Serum Leptin on Weight Gain Induced by Olanzapine in Female Patients with Schizophrenia

Background

Olanzapine (OLZ) treatment is associated with a high risk of weight gain, and may cause abnormalities in glycolipid metabolism. Therefore, the underlying mechanism of OLZ-related weight gain is needed to clarify but not yet been adequately determined. In recent years, adipocytokines such as leptin, adiponectin, and tumor necrosis factor (TNF)-α, which play important roles in energy homeostasis, have been suggested as biomarkers of weight gain. Here, we determined if baseline plasma concentrations of leptin, adiponectin, and TNF-α predict weight gain following OLZ treatment.

Methods

We recruited 31 schizophrenia outpatients (12 men and 19 women, 28.8 ± 10.2 years old) that were unmedicated or on another antipsychotic monotherapy medication. Baseline body mass index (BMI) and plasma levels of leptin, adiponectin, and TNF-α were obtained. All patients started or were switched to OLZ monotherapy for a maximum of 1 year. BMI was also obtained at the endpoint.

Results

Mean BMI change following OLZ treatment was 2.1 ± 2.7 kg/m². BMI change from baseline to endpoint negatively-correlated with baseline leptin levels in female patients (r = −0.514, P = 0.024), but not male patients. Baseline adiponectin or TNF-α levels were not correlated with BMI change.

Conclusion

Baseline plasma leptin can have an effect on subsequent weight gain following OLZ treatment in female patients with schizophrenia.     

The Relationship of Rapid Weight Gain in Infancy to Obesity and Skeletal Maturity in Childhood

Objective: Children with birth weight appropriate for gestational age (AGA) who also demonstrate rapid weight gain in infancy have a greater risk of being overweight or obese during childhood. A concurrent advancement in skeletal maturity would account for their greater size and would, therefore, not necessarily pose a threat of greater risk during adolescence and early adulthood. This study aims to determine whether children with rapid weight gain during infancy have advanced skeletal maturity during childhood. Research Methods and Procedures: One hundred and ninety‐three African children (boys = 108; girls = 85) of normal birth weight and gestational age were assessed from birth to 9 years. Body composition was assessed at 9 years of age by whole‐body DXA, and skeletal maturity was assessed using the Tanner‐Whitehouse II technique. Rapid weight gain in infancy was defined as a +0.67 change in weight‐for‐age Z‐score between birth and 2 years. Results: Rapid weight gain was experienced by over 20% of the sample. Children with rapid weight gain were significantly lighter at birth and significantly taller, heavier, and fatter throughout childhood. Chronological age and Tanner‐Whitehouse II technique skeletal ages at 9 years were not significantly different between groups or between sexes within groups. Discussion: Because AGA children with rapid weight gain have a greater risk of overweight and obesity but are not advanced in skeletal maturity, later adolescent adjustments toward average weight and fatness values are unlikely. The identification and monitoring of such children is of importance in reducing their risk of morbidity.     

Hyperadiponectinemia in Newborns: Relationship with Leptin Levels and Birth Weight

Objective: Adiponectin is the only adipose‐specific hormone that, despite its exclusive production by adipose tissue, is reduced in obesity and is inversely correlated with leptin levels in adults. The aim of this study was to evaluate the adiponectin concentration in umbilical cord blood at different gestational ages and to investigate its possible associations with leptin levels and birth weight. Research Methods and Procedures: Umbilical cord blood was obtained from 132 newborns (male = 65, female = 67, gestational age: 35 to 42 weeks). The anthropometric variables of the newborns studied were birth weight, birth length, body weight/body length, and ponderal index. Adiponectin, insulin, and leptin levels were measured by radioimmunoassay methods. Results: Adiponectin levels in males were not different from those in females (24.10 ± 0.81 vs. 25.62 ± 0.84 μg/mL, p = 0.280). Adiponectin concentrations were positively correlated with birth weight (p < 0.05), birth length (p < 0.05), body weight/body length (p < 0.05), gestational age (p < 0.01), and leptin levels (p < 0.01). Discussion: These findings indicate that adiponectin is present in umbilical cord blood after 35 to 42 weeks of gestation, with higher levels than those usually found in adults, no gender differences, and a positive correlation with birth weight and leptin. These results suggest that not only could neonatal hyperadiponectinemia be associated with the increase of adiponectin production by fetal adipose tissue but also with a possible reduction in an unknown mechanism related to the suppression of adiponectin observed in adults.     

高龄孕妇分娩新生儿出生体重及出院转归的影响因素分析

摘要 目的：探讨高龄孕妇分娩新生儿出生体重及出院转归的影响因素。方法：选择2021年01月到2022年01月与我院就诊的198例产妇作为研究对象,根据孕妇分娩时的年龄分为观察组和对照组,分娩时年龄满35周岁为高龄产妇组（98例）,分娩时年龄为20~34周岁为适龄组（100例）。比较适龄孕妇和高龄孕妇新生儿出生体重情况和新生儿住院时间,对高龄孕妇新生儿体重和新生儿出院转归影响因素进行Logistic单因素分析和多因素分析。结果：与适龄孕妇相比,高龄孕妇新生儿低出生体重儿、巨大儿发生率更高（P<0.05）,新生儿住院时间明显更长（P<0.05）。对高龄孕妇新生儿体重进行单因素分析结果显示,妊娠糖尿病、产检检查、分娩方式、是否使用催产素、分娩时麻醉方式和脐带情况与高龄孕妇新生儿体重无关（P>0.05）,孕妇年龄、孕前BMI、孕期体重增加情况、妊娠高血压、合并其他疾病状况、孕次、产次、羊水情况与高龄孕妇新生儿体重相关（P<0.05）。进行Logistic多因素回归分析结果显示,孕妇年龄、孕前BMI、孕期体重增加情况、孕次、产次、羊水情况是影响高龄孕妇新生儿出生体重的独立危险因素（P<0.05）。对新生儿出院转归情况进行单因素分析结果显示,胎次、开奶时间、喂养方式和有无接受治疗与新生儿出院转归无相关性（P>0.05）,胎龄、出生体重、Apgar评分、出生窒息史、有无伴发疾病与新生儿转归相关（P<0.05）。进行Logistic多因素分析结果显示,胎龄、出生体重、Apgar评分、出生窒息史、有无伴发病是影响新生儿出院转归的独立危险因素（P<0.05）。结论：孕妇年龄、孕前BMI、孕期体重增加情况、孕次、产次、羊水情况是影响高龄孕妇新生儿出生体重的独立危险因素。新生儿出院转归受到胎龄、出生体重、Apgar评分、出生窒息史、有无伴发病影响。