scholarly journals Genetic aspects of metabolic disorders in pregnant women with pathological weight gain

2019 ◽  
Vol 10 (3) ◽  
pp. 271-275
Author(s):  
S. O. Ostafiichuk
Keyword(s):  
Weight Gain ◽  
Pregnant Women ◽  
Leptin Receptor ◽  
Metabolic Diseases ◽  
Receptor Gene ◽  
Insulin Level ◽  
Late Pregnancy ◽  
Serum Levels ◽  
Leptin Resistance ◽  
Enzyme Linked Immunosorbent Assay

Polymorphism of the leptin receptor gene (LEPR) has been shown to be linked to obesity-related metabolic markers and phenotype. Therefore, we hypothesized that the Gln233Arg LEPR polymorphism is related to metabolic changes in pregnancy and the risk of excessive gestational weight gain (GWG). A total of 97 pregnant women with a singleton gestation were enrolled from April 2016 until December 2018. Genetic variants of LEPR were analyzed by real-time polymerase chain reaction, leptin by enzyme-linked immunosorbent assay, lipid profile, and carbohydrate status were assessed in the first, and third trimesters of pregnancy. The recommended GWG was diagnosed in 34.0%, insufficient in 19.6%, and excessive in 46.4% patients. Statistical analysis revealed that 20.6% patients were with AA genotype, 50.5% – AG genotype, and 28.9% – GG genotype. The frequency of GG-alleles carriers of the LEPR Gln233Arg gene in the group of excessive GWG patients was 3 times higher compared to recommended GWG patients. Thus, the inheritance of pathological G-homozygotes increases the risk of excessive weight gain by 7 times, compared to carriers of the AA genotype. LEPR GG polymorphism was significantly associated with high levels of triglycerides, total cholesterol, lipoprotein low and very low density, and leptin compared to homozygous А-carriers in the third trimester of pregnancy. In pregnant women with GG polymorphism, the glucose level, insulin level, and HOMO-IR index were significantly increased compared to women with AA genotype in late pregnancy. In the group with excessive GWG, the presence of GG-alleles of the LEPR gene was accompanied by a higher level of hyperleptinemia, compared to carriers of AA-genotype. Inheritance of pathological G-homozygotes was associated with hyperlipidemia, leptin resistance with high leptin serum levels, and increased insulin resistance, which was especially manifested in excessive GWG. In our opinion, excessive GWG can be seen as a marker of the mother's genotype and genetic predisposition to the development of metabolic diseases after delivery.

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

2003 ◽  
Vol 11 (3) ◽  
pp. 377-386 ◽  
Author(s):  
Caroline T.M. van Rossum ◽  
Barbara Hoebee ◽  
Marleen A. van Baak ◽  
Monica Mars ◽  
Wim H.M. Saris ◽  
...  
Keyword(s):  
Genetic Variation ◽  
Weight Gain ◽  
Leptin Receptor ◽  
Receptor Gene

Greater energy demand of exercise during pregnancy does not impact mechanical efficiency

2020 ◽  
Vol 45 (5) ◽  
pp. 493-499 ◽  
Author(s):  
Kathryn M. Denize ◽  
Pegah Akbari ◽  
Danilo Fernandes da Silva ◽  
Francois Haman ◽  
Kristi B. Adamo
Keyword(s):  
Physical Activity ◽  
Weight Gain ◽  
Pregnant Women ◽  
Gestational Weight Gain ◽  
Energy Demand ◽  
Movement Pattern ◽  
Late Pregnancy ◽  
Mechanical Efficiency ◽  
Moderate Intensity ◽  
Gestational Weight

Pregnant women are recommended to engage in 150 min of moderate-intensity physical activity per week to reduce pregnancy complications. Many women struggle to remain physically active throughout pregnancy, and there is no consensus about whether women adopt a less efficient movement pattern as they progress through pregnancy and experience gestational weight gain. This study assessed the change in energy expenditure and mechanical efficiency in pregnant women (PREG; n = 10) when performing a walking treadmill task in early, mid, and late pregnancy and also compared with an age- and body mass index-matched, nonpregnant (CON; n = 10) group. On average, the PREG group gained within the Institute of Medicine’s gestational weight gain guidelines (11.6 ± 3.6 kg) and were all inactive (measured using accelerometry), except for 1 participant, by the third trimester, as per the 2019 Canadian physical activity guidelines for pregnant women. Energy expended to complete the walking task increased throughout pregnancy and was higher than the controls (111.5 ± 24.6 kcal) in mid and late pregnancy (139.0 ± 22.2 kcal, p = 0.02, and 147.3 ± 24.6 kcal, p = 0.005, respectively), but not early pregnancy (129.9 ± 18.9 kcal, p = 0.08). Walking mechanical efficiency was similar within pregnant women at each time point and compared to nonpregnant controls. Our findings add to the growing body of evidence demonstrating that pregnant women can safely perform physical activity by showing that walking mechanical efficiency is unchanged at low to moderate intensities. Novelty Energy demand during exercise increases proportionally to weight gain across pregnancy trimesters. However, mechanical efficiency remains unchanged during low- to moderate-intensity walking.

Are Anti-β2 Glycoprotein 1 Antibodies Associated with Placenta-Mediated Pregnancy Complications? A Nested Case–Control Study

2018 ◽  
Vol 35 (11) ◽  
pp. 1093-1099 ◽  
Author(s):  
Leslie Skeith ◽  
Karim Abou-Nassar ◽  
Mark Walker ◽  
Tim Ramsay ◽  
Ronald Booth ◽  
...  
Keyword(s):  
Pregnant Women ◽  
Pregnancy Complications ◽  
Case Control Study ◽  
Late Pregnancy ◽  
Case Control ◽  
Immunoglobulin M ◽  
Enzyme Linked Immunosorbent Assay ◽  
Significant Difference ◽  
Antibody Positivity ◽  
Control Study

Background While anti-β2 glycoprotein 1 (anti-β2GP1) antibody positivity is included in the diagnostic criteria for antiphospholipid syndrome (APS), the association between anti-β2GP1 and the obstetrical complications of APS has been inconsistently reported and remains unclear. Objective We completed a case–control study nested within the Canadian Ottawa and Kingston (OaK) Birth Cohort to evaluate the association between anti-β2GP1 antibody positivity and placenta-mediated pregnancy complications. Study Design Five hundred cases were randomly selected among pregnant women who experienced any of the following independently adjudicated placenta-mediated pregnancy complications: preeclampsia, placental abruption, late pregnancy loss (≥ 12 weeks' gestation), and birth of a small-for-gestational age (SGA) infant < 10th percentile. Five hundred pregnant women without any placenta-mediated pregnancy complications were selected as controls. Stored blood samples were analyzed for the presence of anti-β2GP1 antibodies by enzyme-linked immunosorbent assay. Results Anti-β2GP1 immunoglobulin G (IgG) and/or immunoglobulin M (IgM) antibodies in titers ≥ 20 G/M units (> 99th percentile) were present in 24 of 497 (4.8%) of controls and 33 of 503 (6.6%) of cases. There was no significant difference between cases and controls for the composite outcome of any placenta-mediated pregnancy complications (odds ratio, 1.38, 95% confidence interval [CI], 0.8–2.37, p = 0.25). Conclusion Our results call into question the association between anti-β2GP1 antibodies and placenta-mediated pregnancy complications, with further research needed.

scholarly journals Leptin resistance: a prediposing factor for diet-induced obesity

2009 ◽  
Vol 296 (3) ◽  
pp. R493-R500 ◽  
Author(s):  
Philip J. Scarpace ◽  
Yi Zhang
Keyword(s):  
Weight Gain ◽  
Leptin Receptor ◽  
Causative Factor ◽  
Leptin Resistance ◽  
Chow Diet ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Dietary Fructose ◽  
Complex Chronic Disease ◽  
Obesity Syndrome

Obesity is a resilient and complex chronic disease. One potential causative factor in the obesity syndrome is leptin resistance. Leptin behaves as a potent anorexic and energy-enhancing hormone in most young or lean animals, but its effects are diminished or lacking in the obese state associated with a normal genetic background. Emerging evidence suggests that leptin resistance predisposes the animal to exacerbated diet-induced obesity (DIO). Elevation of central leptin in young, lean rats induces a leptin resistance that precludes obesity on a chow diet but accelerates high-fat (HF)-induced obesity. Similarly, chronic dietary fructose consumption evokes a leptin resistance that causes obesity only upon HF exposure. Inherent central leptin insensitivity also contributes to dietary weight gain in certain obesity-prone rats. Conversely, aged, leptin-resistant animals are obese with continuous chow feeding and demonstrate aggravated obesity when challenged with an HF diet. Additionally, a submaximal central blockade with a leptin antagonist leads to obesity on both chow and HF diets, as is the case in rodents with leptin receptor deficiency of genetic origin. Despite the differences in the incidence of obesity on a chow diet, all of these forms of leptin resistance predispose rodents to aggravated HF-mediated obesity. Moreover, once leptin resistance takes hold, it aggravates DIO, and the leptin resistance and obesity compound one another, promoting a vicious cycle of escalating weight gain.

scholarly journals Sleep Patterns in Pregnant Women with Obesity Differentially Affect Energy Intake and Metabolic Health

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 984-984
Author(s):  
Emily Flanagan ◽  
Abby Altazan ◽  
Jasper Most ◽  
Robbie Beyl ◽  
Daniel Hsia ◽  
...  
Keyword(s):  
Weight Gain ◽  
Pregnant Women ◽  
Energy Intake ◽  
Early Pregnancy ◽  
Late Pregnancy ◽  
Sleep Time ◽  
Metabolic Health ◽  
Sleep Patterns ◽  
Gestational Weight ◽  
Gain Energy

Abstract Objectives During pregnancy, altered glucose kinetics coupled with disrupted sleep increase the risk for adverse metabolic health outcomes. The aim of this prospective, observational study in pregnant women with obesity was to 1) examine sleep patterns in early and late pregnancy; and 2) identify how changes in sleep patterns impact gestational weight gain, energy intake and metabolic health. Methods In 52 healthy pregnant women with obesity (27.4 ± 0.6 y; BMI: 36.3 ± 0.7 kg/m,2), energy intake (intake-balance method), and changes in weight, fasting glucose, insulin, lipids and habitual sleep (5 consecutive nights via wrist worn accelerometer) were assessed from early (13,0–15,6 weeks) to late (35,0–36,6) pregnancy. A change to habitual sleep parameters (increase or decrease) was defined as ± one-half of the standard deviation of the 5-day measurement in early pregnancy. Results Results In early pregnancy, time spent in bed (TIB) was 9.40 ± 0.13 h and varied 1.61 ± 0.11 h across the 5 nights. Total sleep time (TST) and sleep efficiency (SE) significantly declined from early to late pregnancy 7.05 ± 0.13 h to 6.46 ± 0.15 h (P &lt; 0.001) and 76 ± 0.1% to 71 ± 0.2% (P &lt; 0.001), respectively. Women who increased TIB (11 of 52) had a significant decrease in plasma glucose −11.6 ± 4.3% (P &lt; 0.01) and a trend towards lower insulin (−57.8 ± 33.5%; P = 0.09) and HOMA-IR (−72.4 ± 37.3%; P = 0.058) across pregnancy compared to women who decreased their TIB (13 of 52). Women who increased TIB had a significantly lower daily energy intake (−540 ± 163 kcal; P &lt; 0.01) and tended to have less gestational weight gain (−146.7 ± 87.6 g/wk; P = 0.10). There was no difference in weight gain, energy intake or plasma markers between women who increased or decreased TST or SE. Conclusions Although sleep time and sleep quality decline throughout pregnancy, TIB had the greatest impact on metabolic health in pregnant women with obesity. Women spending more TIB consumed fewer calories. Our data suggest that the relationship between glucose metabolism and sleep during pregnancy is at least in part explained by lower energy intakes, possibly due to shorter eating windows. Studies that manipulate the eating window, independent of sleep timing are needed to understand the benefits to metabolic health for women during pregnancy. Funding Sources National Institutes of Health [R01DK099175].

scholarly journals Association Between Diet Quality & Rate of Gestational Weight Gain Among Pregnant Women in Dhulikhel, Nepal

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1089-1089
Author(s):  
Kelly Tiderencel ◽  
Joachim Sackey ◽  
Diane Rigassio-Radler ◽  
Emily Barrett ◽  
Archana Shrestha ◽  
...  
Keyword(s):  
Weight Gain ◽  
Pregnant Women ◽  
Gestational Weight Gain ◽  
Diet Quality ◽  
A Priori ◽  
Late Pregnancy ◽  
Red Meat ◽  
Food Groups ◽  
Gestational Weight ◽  
The Mean

Abstract Objectives The National Academy of Medicine (NAM) guidelines recommend linear gestational weight gain (GWG) in the 2nd and 3rd trimester with appropriate rate defined based on pre-pregnancy BMI. Here we prospectively examined the association between diet quality and GWG rate from 2nd to 3rd trimester among women receiving prenatal care in a periurban hospital in Nepal. Methods A pilot cohort of singleton pregnant women (N = 101; age 25.9 ± 4.1 years) was recruited from a tertiary, periurban hospital in Nepal. In the 1st trimester, diet quality was assessed from the adapted Nepali version of the PrimeScreen questionnaire, which assigned diet quality scores (range 0–42; higher scores for better quality) based on consumption frequency of 12 healthy and 9 unhealthy food groups. The GWG rate was calculated as the measured weight at the early-to-mid 3rd trimester (28–35 wks) minus the weight at 2nd trimester (13–25 wks), divided by the number of weeks in between. Linear regression estimated the association between diet quality and GWG rate, adjusting for a priori covariates including age, education, ethnicity, pre-pregnancy BMI, and nausea/vomiting. The adequacy of GWG rate was also categorized as inadequate, adequate, or excessive using NAM guidelines. Results Most women were of normal (55.4%) or overweight (33.7%) BMI status pre-pregnancy. The mean GWG rate in mid-to-late pregnancy was 0.46 ± 0.2 kg/wk and the mean diet quality score was 23.6 ± 2.5. Based on pre-pregnancy BMI, 49.4% of women had excessive GWG rate, while nearly equal numbers had either adequate GWG or inadequate GWG rate. Pre-pregnancy BMI and GWG rate were inversely correlated (r = −0.21, P = 0.049). Education level was positively associated with both GWG rate (P = 0.01) and adequacy of GWG (P = 0.02). There was no significant association between diet quality and the GWG rate [adjusted β (95% CI) = −0.02 (−0.05, 0.01); P = 0.14]. The mean GWG rate was marginally lower (0.44 vs. 0.57 kg/wk; P = 0.06) among those with high versus low (2 + servings vs. 0–1 serving/wk) intake of red meat; similar findings were seen when comparing red meat intake between women with excessive versus adequate GWG (Cramer's V = 0.2; P = 0.06). Conclusions While overall diet quality is not related to GWG among Nepali women, a high intake of red meat may be a potential risk factor for excessive GWG in this population. Funding Sources Rutgers Global Health Institute.

scholarly journals Persistent organic pollutants in pregnant women potentially affect child development and thyroid hormone status

2021 ◽  
Author(s):  
Anna A. Krönke ◽  
Anne Jurkutat ◽  
Maike Schlingmann ◽  
Tanja Poulain ◽  
Matthias Nüchter ◽  
...  
Keyword(s):  
Weight Gain ◽  
Thyroid Hormone ◽  
Pregnant Women ◽  
Postnatal Development ◽  
Organic Pollutants ◽  
Persistent Organic Pollutants ◽  
Serum Levels ◽  
Maternal Serum ◽  
Hormone Status ◽  
Mother And Child

Abstract Background Potentially harmful effects of persistent organic pollutants (POPs) such as polychlorinated biphenyls (PCBs) and dichlorodiphenyltrichloroethane (DDT) on prenatal development and the endocrine system have been controversially discussed. Methods Working with a German cohort of 324 pregnant women, we assessed POP levels and used robust linear regression models to determine potential associations between maternal POP concentrations and pre- and postnatal development in the children, as well as the thyroid hormone status of the mother and child. Results Maternal p,p′-dichlorodiphenyldichloroethylene (p,p′-DDE) and most measured PCBs positively correlated with postnatal weight gain. We detected no correlation between newborn birth weight and head circumference, respectively, and maternal PCB and p,p′-DDE serum levels, while body length at birth was negatively associated with the maternal serum concentration of PCB 183. Maternal p,p′-DDE and nearly all PCB serum levels showed a negative correlation with maternal free triiodothyronine (FT3). p,p′-DDE and PCB 74 and 118 were negatively associated with maternal thyroid-stimulating hormone levels. In addition, we identified significant associations between maternal POP levels and thyroid hormone parameters of the child. Conclusions These results indicate that POP exposure likely affects different aspects of pre- and postnatal development and impacts the thyroid hormone status of both mother and child. Impact Pregnant women in a German cohort display a substantial accumulation of POPs. Body mass index and age influence maternal serum POP levels. Maternal POP levels show correlations with the child’s length at birth and weight gain, and FT3 levels in the mother and child. Our data provide additional evidence for the potentially harmful influence of POPs. Our data indicate that POPs influence pre- and postnatal development.

Abstract 25: Angiotensin AT 1A Receptors on Leptin Receptor-Expressing Cells are Required for the Blood Pressure and Metabolic Rate Effects of Leptin

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Justin L Grobe ◽  
Kristin E Claflin
Keyword(s):  
Blood Pressure ◽  
Metabolic Rate ◽  
Body Mass ◽  
Leptin Receptor ◽  
Receptor Gene ◽  
Brain Regions ◽  
Leptin Resistance ◽  
Brown Adipose ◽  
Obesity Hypertension ◽  
The Brain

Circulating leptin and the local brain renin-angiotensin system (RAS) both contribute to the control of food intake (FI), resting metabolic rate (RMR) and blood pressure (BP), and both have been postulated to contribute to obesity-hypertension. Here we examined the provocative hypothesis that the brain RAS is required for (or mediates) the RMR- and BP-stimulating effects of leptin. To create animals lacking the AT 1A receptor specifically in cells expressing the leptin receptor (“KO”), mice with a flox’ed version of the endogenous angiotensin AT 1A receptor gene (AT 1A flox ) were crossed with mice expressing cre-recombinase via the leptin receptor promoter (ObR-Cre). Body mass, body composition, blood chemistry, glucose tolerance, and FI behaviors were essentially unchanged through 34 weeks of age in mice maintained on standard chow (Teklad 7013). In contrast, anesthetized BP (MAP; control n=9, 91.6 ± 4.1, vs KO n=8, 78.0 ± 3.7 mmHg) and heart rate (351 ± 13, vs 308 ± 11 BPM) were reduced in KO mice (both P<0.05). Further, interscapular brown adipose (BAT SNA, 112 ± 22, vs 22 ± 35 % above baseline at 3 hr) and renal (154 ± 19, vs 53 ± 23 % above baseline at 3 hr) sympathetic nerve activity responses to acute leptin injection (60 μg, i.v.) were completely abolished (both P<0.05). When maintained on a 45% high fat diet (OpenSource D12451 ) to increase endogenous leptin production, KO mice exhibited accelerated body mass (control n=15, -0.1 ± 0.1, vs KO n=4, +1.7 ± 0.5 g/wk) and fat mass (+2.9 ± 0.5, vs +4.9 ± 1.1 g/5 wk) gains (both P<0.05), likely due to normal FI behaviors but a 18% reduction in RMR (control n=16, 0.196 ± 0.011, vs KO n=7, 0.161 ± 0.004 kcal/hr at 30°C, P<0.05). We conclude that expression of angiotensin AT 1A receptors on leptin-sensitive cells is required for the metabolic rate and cardiovascular effects of leptin. Ongoing studies are focused on identifying the brain regions and subsets of leptin receptor-expressing cells in which this RAS-leptin cross-talk occurs, and the directionality and molecular mediators of this interaction. We hypothesize that uncontrolled or pathological activity of the brain RAS may thus help explain the clinically variable effects of leptin, and contribute to the mechanism(s) of selective leptin resistance and obesity-hypertension.

scholarly journals Polymorphisms of Leptin (-2548 G/A) and Leptin Receptor (Q223R) Genes in Iranian Women with Breast Cancer

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Reza Mahmoudi ◽  
Bahareh Noori Alavicheh ◽  
Mohammad Amin Nazer Mozaffari ◽  
Mohammad Fararouei ◽  
Mohsen Nikseresht
Keyword(s):  
Breast Cancer ◽  
Significant Contribution ◽  
Leptin Receptor ◽  
Receptor Gene ◽  
Serum Levels ◽  
Serum Leptin ◽  
Increased Risk ◽  
Pcr Rflp ◽  
The Mean ◽  
Larger Sample

Recent studies have shown that polymorphisms in leptin and leptin receptor genes are associated with increased risk for breast cancer. This study aimed at investigating -2548 G/A polymorphism in leptin gene and Q223R polymorphism in leptin receptor gene in patients with breast cancer. The study included 45 women with breast cancer and 41 healthy women. PCR-RFLP was used to determine the genotype of the subjects in terms of -2548 G/A polymorphism in leptin gene and Q223R polymorphism in leptin receptor gene. Serum levels of leptin were also measured by ELISA. For -2548 G/A polymorphism, the genotypes were homozygous AA (OR = 1.13;p=0.8) and heterozygous GA (OR = 0.41;p=0.2) and for Q223R polymorphism, the genotypes were homozygous RR (OR = 6.7;p=0.09) and heterozygous QR (OR = 8.3;p=0.06). The mean serum level of leptin was 33.22 ± 21.35 ng/mL in patients and 29.49 ± 23.27 ng/mL in the normal participants (p=0.3). Although, despite the magnitude of the associations, the results suggested no statistically significant contribution of -2548 G/A polymorphism (in leptin gene), Q223R polymorphism (in leptin receptor gene), and serum leptin levels in predicting the risk of breast cancer, further studies with larger sample size are suggested.

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