| 1. |
- Bentham, James, et al.
(författare)
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A century of trends in adult human height
- 2016
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Ingår i: eLIFE. - 2050-084X. ; 5
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Tidskriftsartikel (refereegranskat)abstract
- Being taller is associated with enhanced longevity, and higher education and earnings. We reanalysed 1472 population-based studies, with measurement of height on more than 18.6 million participants to estimate mean height for people born between 1896 and 1996 in 200 countries. The largest gain in adult height over the past century has occurred in South Korean women and Iranian men, who became 20.2 cm (95% credible interval 17.522.7) and 16.5 cm (13.319.7) taller, respectively. In contrast, there was little change in adult height in some sub-Saharan African countries and in South Asia over the century of analysis. The tallest people over these 100 years are men born in the Netherlands in the last quarter of 20th century, whose average heights surpassed 182.5 cm, and the shortest were women born in Guatemala in 1896 (140.3 cm; 135.8144.8). The height differential between the tallest and shortest populations was 19-20 cm a century ago, and has remained the same for women and increased for men a century later despite substantial changes in the ranking of countries.
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| 2. |
- Bentham, James, et al.
(författare)
-
A century of trends in adult human height
- 2016
-
Ingår i: eLIFE. - : eLife Sciences Publications Ltd. - 2050-084X. ; 5
-
Tidskriftsartikel (refereegranskat)abstract
- Being taller is associated with enhanced longevity, and higher education and earnings. We reanalysed 1472 population-based studies, with measurement of height on more than 18.6 million participants to estimate mean height for people born between 1896 and 1996 in 200 countries. The largest gain in adult height over the past century has occurred in South Korean women and Iranian men, who became 20.2 cm (95% credible interval 17.5–22.7) and 16.5 cm (13.3– 19.7) taller, respectively. In contrast, there was little change in adult height in some sub-Saharan African countries and in South Asia over the century of analysis. The tallest people over these 100 years are men born in the Netherlands in the last quarter of 20th century, whose average heights surpassed 182.5 cm, and the shortest were women born in Guatemala in 1896 (140.3 cm; 135.8– 144.8). The height differential between the tallest and shortest populations was 19-20 cm a century ago, and has remained the same for women and increased for men a century later despite substantial changes in the ranking of countries.
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| 3. |
- Gonzalez-Granillo, Marcela, et al.
(författare)
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Sex-specific lipid molecular signatures in obesity-associated metabolic dysfunctions revealed by lipidomic characterization in ob/ob mouse
- 2019
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Ingår i: Biology of Sex Differences. - : BMC. - 2042-6410. ; 10
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Tidskriftsartikel (refereegranskat)abstract
- The response to overfeeding is sex dependent, and metabolic syndrome is more likely associated to obesity in men or postmenopausal women than in young fertile women. We hypothesized that obesity-induced metabolic syndrome is sex dependent due to a sex-specific regulation of the fatty acid (FA) synthesis pathways in liver and white adipose depots. We aimed to identify distinctive molecular signatures between sexes using a lipidomics approach to characterize lipid species in liver, perigonadal adipose tissue, and inguinal adipose tissue and correlate them to the physiopathological responses observed. Males had less total fat but lower subcutaneous on visceral fat ratio together with higher liver weight and higher liver and serum triglyceride (TG) levels. Males were insulin resistant compared to females. Fatty acid (FA) and TG profiles differed between sexes in both fat pads, with longer chain FAs and TGs in males compared to that in females. Remarkably, hepatic phospholipid composition was sex dependent with more abundant lipotoxic FAs in males than in females. This may contribute to the sexual dimorphism in response to obesity towards more metaflammation in males. Our work presents an exhaustive novel description of a sex-specific lipid signature in the pathophysiology of metabolic disorders associated with obesity in ob/ob mice. These data could settle the basis for future pharmacological treatment in obesity.
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| 4. |
- Hases, Linnea, et al.
(författare)
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High-fat diet and estrogen impacts the colon and its transcriptome in a sex-dependent manner
- 2020
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Ingår i: Scientific Reports. - : Springer Nature. - 2045-2322. ; 10
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Tidskriftsartikel (refereegranskat)abstract
- There is a strong association between obesity and colorectal cancer (CRC), especially in men, whereas estrogen protects against both the metabolic syndrome and CRC. Colon is the first organ to respond to high-fat diet (HFD), and estrogen receptor beta (ERβ) can attenuate CRC development. How estrogen impacts the colon under HFD and related sex differences has, however, not been investigated. To dissect this, mice were fed control diet or HFD for 13 weeks and administered receptor-selective estrogenic ligands for the last three weeks. We recorded impact on metabolism, colon crypt proliferation, macrophage infiltration, and the colon transcriptome. We found clear sex differences in the colon transcriptome and in the impact by HFD and estrogens, including on clock genes. ERα-selective activation reduced body weight and generated systemic effects, whereas ERβ-selective activation had local effects in the colon, attenuating HFD-induced macrophage infiltration and epithelial cell proliferation. We here demonstrate how HFD and estrogens modulate the colon microenvironment in a sex- and ER-specific manner.
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| 5. |
- Savva, Christina
(författare)
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Maternal obesity and offspring metabolic outcomes : focus on sex differences
- 2022
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Obesity is a worldwide health issue affecting all ages and both sexes, and its prevalence is progressively increasing among adults and children. The predisposition to metabolic complications caused by obesity is sex dependent. Intrauterine environmental changes such as overnutrition before conception, during pregnancy and lactation, have been recognized as factors predisposing offspring to metabolic complications later in life. Interestingly, sex specific differences in the adaptation to maternal obesity have been observed, but the underlying mechanism is still unclear. The general aim of the current thesis was to investigate the sexual dimorphism in metabolism during obesity and to elucidate the sex-dependent impact of maternal obesity on offspring, with particular emphasis on liver and adipose tissue metabolism. For this purpose, we used a combination of both in vivo and ex vivo advanced techniques, including nuclear magnetic resonance, transcriptomic and lipidomic analysis in key tissues regulating lipid metabolism; namely liver, subcutaneous (SAT), visceral (VAT), and brown (BAT) adipose tissues. In PAPER I we investigated the sex-specific response to obesity-induced metabolic syndrome and aimed to identify sex-specific characteristic lipid molecular species in liver, VAT and SAT in female and male ob/ob mice. We showed that upon overfeeding, males accumulated less total fat with a distribution towards more VAT and less SAT compared to females. Males presented higher lipid accumulation in liver and circulating lipids and were more insulin resistant compared to females. Males induced inflammation in adipose tissue while females presented higher pro-inflammatory markers in liver in response to overeating. Furthermore, the fatty acid and triglyceride profile in both adipose depots were diverse between the two sexes. Males had longer chain fatty acids and triglycerides compared to females. Additionally, here we showed that the hepatic phospholipid profile was sex- dependent with more abundant lipotoxic fatty acids in males than in females. The fatty acid and triglyceride synthesis pathways was highly sex-dependent at the transcriptional level, which may contribute to the sex-dependent metabolic profile. Our results provide a unique description of sexual dimorphic lipid profile in metabolic organs corelated to obesity and could be a contribution for future and more precise treatment of obesity. In PAPER II we investigated the sex-dependent long-term adaptation to maternal obesity in offspring on control diet after weaning with focus on the liver. Males from obese mothers had higher adiposity and were more insulin resistant at short-term but on the long-term post- weaning control diet reversed these effects. Our results demonstrated that maternal obesity influenced differently the hepatic lipid synthesis pathways in female and male offspring and caused a more dysfunctional metabolic profile in males than in females. We observed a sex- specific alteration in the fatty acid, triglyceride, and phospholipid profile together with a sex- specific transcriptional regulation of metabolic pathways in liver. In PAPER III we explored how maternal obesity can predispose white and brown adipose tissue in obese offspring to metabolic dysfunctions in the long-term. We showed that in utero high fat diet environment in offspring on obesogenic diet, altered the triglyceride profile between adipose depots and sexes. Maternal obesity caused changes in triglyceride composition in SAT and BAT and increased the thermogenic activity in BAT in female offspring only. In males, maternal obesity caused whitening of BAT and increased the adipocyte number in VAT and generally impaired their metabolic profile. Our results show that maternal obesity programs the transcriptional activity in white and brown adipose tissue in a sex- and adipose depot- dependent manner. The PAPER IV is a continuation of the study in PAPER III where we investigated the sex- dependent metabolic response to maternal obesity in offspring on obesogenic diet with special focus on liver. Here we showed that maternal obesity caused hepatic insulin resistance in females, and hepatic steatosis and inflammation in males. Moreover, we observed that maternal obesity caused changes in the transcriptional activity and triglyceride profile in female offspring that might prevent the adverse effects of in utero exposure to obesity. In conclusion, our results demonstrate that there is an in utero metabolic programming in offspring born from obese mothers that is sex and tissue specific. Given that the prevalence of obesity among women of reproductive age is increasing drastically, it is crucial to better define the in utero changes in offspring and its consequences. An important outcome of studying the sex differences in offspring metabolism is to understand the underlying mechanisms and paved the way to precision medicine to develop potential interventions and tackle future diseases in subsequent generations.
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| 6. |
- Savva, Christina, et al.
(författare)
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Molecular programming modulates hepatic lipid metabolism and adult metabolic risk in the offspring of obese mothers in a sex-specific manner
- 2022
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Ingår i: Communications Biology. - : Springer Nature. - 2399-3642. ; 5:1
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Tidskriftsartikel (refereegranskat)abstract
- Male and female offspring of obese mothers are known to differ extensively in their metabolic adaptation and later development of complications. We investigate the sex-dependent responses in obese offspring mice with maternal obesity, focusing on changes in liver glucose and lipid metabolism. Here we show that maternal obesity prior to and during gestation leads to hepatic steatosis and inflammation in male offspring, while female offspring are protected. Females from obese mothers display important changes in hepatic transcriptional activity and triglycerides profile which may prevent the damaging effects of maternal obesity compared to males. These differences are sustained later in life, resulting in a better metabolic balance in female offspring. In conclusion, sex and maternal obesity drive differently transcriptional and posttranscriptional regulation of major metabolic processes in offspring liver, explaining the sexual dimorphism in obesity-associated metabolic risk.
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