In utero programming of later adiposity: The role of fetal growth restriction

Intrauterine growth restriction (IUGR) is strongly associated with obesity in adult life. The mechanisms contributing to the onset of IUGR-associated adult obesity have been studied in animal models and humans, where changes in fetal adipose tissue development, hormone levels and epigenome have been identified as principal areas of alteration leading to later life obesity. Following an adverse in utero development, IUGR fetuses display increased lipogenic and adipogenic capacity in adipocytes, hypoleptinemia, altered glucocorticoid signalling, and chromatin remodelling, which subsequently all contribute to an increased later life obesity risk. Data suggest that many of these changes result from an enhanced activity of the adipose master transcription factor regulator, peroxisome proliferator-activated receptor-γ (PPARγ) and its coregulators, increased lipogenic fatty acid synthase (FAS) expression and activity, and upregulation of glycolysis in fetal adipose tissue. Increased expression of fetal hypothalamic neuropeptide Y (NPY), altered hypothalamic leptin receptor expression and partitioning, reduced adipose noradrenergic sympathetic innervations, enhanced adipose glucocorticoid action, and modifications in methylation status in the promoter of hepatic and adipose adipogenic and lipogenic genes in the fetus also contribute to obesity following IUGR. Therefore, interventions that inhibit these fetal developmental changes will be beneficial for modulation of adult body fat accumulation. © 2012 Ousseynou Sarr et al

Glucagon-like peptide-1 receptor agonist versus basal insulin in type-2 diabetic patients: An efficacy and safety analysis

Purpose: To compare the effectiveness of glucagon-like peptide 1 receptor agonist with that of basal insulin in type 2 diabetes patients. Methods: Type-2 diabetes patients who were insensitive to metformin were treated with glucagon-like peptide 1 receptor agonist (GP cohort, n = 115) or basal insulin (BI cohort, n = 152) with metformin. Hemoglobin A1c (HbA1c) level and body weight were determined, and adverse effects also recorded. Results: After 16 weeks of treatment, glucagon-like peptide 1 receptor agonist did not significantly reduce HbA1c levels (7.45 ± 2.11 % vs. 7.01 ± 2.01, p = 0.107). In contrast, basal insulin significantly reduced the levels of HbA1c (7.91 ± 2.98 % vs. 7.13 ± 2.22 %, p = 0.010, q = 3.852). Glucagon-likepeptide 1 receptor agonist reduced the body weight of patients (65.25 ± 7.55 kg vs. 62.16 ± 6.15 kg, p = 0.0008, q = 5.121), unlike basal insulin (63.71 ± 6.15 vs. 62.65 ± 6.76 kg, p = 0.154). Conclusion: Glucagon-like peptide 1 receptor agonist and basal insulin + metformin produce identical effectiveness in the treatment of type-2 diabetic patients. Keywords: Glucagon-like peptide-1 receptor agonist, Glycemic control, Insulin, Metformin, Type-2 diabete

Dietary treatment with omega fatty acids mediates in vitro rumen fermentation kinetics and reduce methane emission in water buffalo

Purpose: To investigate the effect of dietary supplementation of two omega fatty acids on in vitro rumen  fermentation, microbial populations, total gas and methane (CH4) production．Methods: Both linoleic and linolenic acids were supplemented at 0 (control), 1, 3, 5 and 7 % of dry matter (DM) in a ration with a high roughage to concentrate ratio (70: 30). Total gas and CH4  were measured at 3, 6, 9, 12 and 24 h of fermentation while pH, volatile fatty acids (VFA), and ammonia nitrogen (NH3-N) concentrations were measured at 24 h using buffalo rumen fluid in an in vitro batch culture system. Microbial populations were determined using 16S-rDNA gene primers by RT-PCR.Results: The results revealed that linoleic acid at 3, 5 and 7 % decreased the concentration of NH3-N (p< 0.05) but linolenic acid at 5 and 7 % increased NH3-N (p < 0.05). A linear decrease (p <0.001) in acetate and butyrate, coupled with linear increase (p <0.001) in propionate was observed in response to treatment. Furthermore, supplementation of 3, 5 and 7 % of both fatty acids linearly (p < 0.001) decreased total gas and CH4 production when compared to the control. The addition of linoleic acid linearly (p < 0.001) decreased the number of protozoa without affecting methanogens, while linolenic acid linearly and quadratically (p < 0.001) reduced the population of both protozoa and methanogens (p < 0.05).Conclusion: Linolenic acid is more effective at a 3 % level in reducing methane production (up to 63 %) in high roughage diets

Caffeine Reduces 11β-Hydroxysteroid Dehydrogenase Type 2 Expression in Human Trophoblast Cells through the Adenosine A2B Receptor

Maternal caffeine consumption is associated with reduced fetal growth, but the underlying molecular mechanisms are unknown. Since there is evidence that decreased placental 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) is linked to fetal growth restriction, we hypothesized that caffeine may inhibit fetal growth partly through down regulating placental 11β-HSD2. As a first step in examining this hypothesis, we studied the effects of caffeine on placental 11β-HSD2 activity and expression using our established primary human trophoblast cells as an in vitro model system. Given that maternal serum concentrations of paraxanthine (the primary metabolite of caffeine) were greater in women who gave birth to small-for-gestational age infants than to appropriately grown infants, we also studied the effects of paraxanthine. Our main findings were: (1) both caffeine and paraxanthine decreased placental 11β-HSD2 activity, protein and mRNA in a concentration-dependent manner; (2) this inhibitory effect was mediated by the adenosine A2B receptor, since siRNA-mediated knockdown of this receptor prevented caffeine- and paraxanthine-induced inhibition of placental 11β-HSD2; and (3) forskolin (an activator of adenyl cyclase and a known stimulator of 11β-HSD2) abrogated the inhibitory effects of both caffeine and paraxanthine, which provides evidence for a functional link between exposure to caffeine and paraxanthine, decreased intracellular levels of cAMP and reduced placental 11β-HSD2. Taken together, these findings reveal that placental 11β-HSD2 is a novel molecular target through which caffeine may adversely affect fetal growth. They also uncover a previously unappreciated role for the adenosine A2B receptor signaling in regulating placental 11β-HSD2, and consequently fetal development

Minimal information for studies of extracellular vesicles (MISEV2023): From basic to advanced approaches

Extracellular vesicles (EVs), through their complex cargo, can reflect the state of their cell of origin and change the functions and phenotypes of other cells. These features indicate strong biomarker and therapeutic potential and have generated broad interest, as evidenced by the steady year-on-year increase in the numbers of scientific publications about EVs. Important advances have been made in EV metrology and in understanding and applying EV biology. However, hurdles remain to realising the potential of EVs in domains ranging from basic biology to clinical applications due to challenges in EV nomenclature, separation from non-vesicular extracellular particles, characterisation and functional studies. To address the challenges and opportunities in this rapidly evolving field, the International Society for Extracellular Vesicles (ISEV) updates its 'Minimal Information for Studies of Extracellular Vesicles', which was first published in 2014 and then in 2018 as MISEV2014 and MISEV2018, respectively. The goal of the current document, MISEV2023, is to provide researchers with an updated snapshot of available approaches and their advantages and limitations for production, separation and characterisation of EVs from multiple sources, including cell culture, body fluids and solid tissues. In addition to presenting the latest state of the art in basic principles of EV research, this document also covers advanced techniques and approaches that are currently expanding the boundaries of the field. MISEV2023 also includes new sections on EV release and uptake and a brief discussion of in vivo approaches to study EVs. Compiling feedback from ISEV expert task forces and more than 1000 researchers, this document conveys the current state of EV research to facilitate robust scientific discoveries and move the field forward even more rapidly

Spatial Spillover Effects of Urbanization on Ecosystem Services under Altitude Gradient

Rapid urbanization has made mountain development an important means to alleviate the shortages of construction land on plains, which has significantly affected regional ecosystem services. In-depth research on the impact of urbanization on ecosystem services under altitude gradients is of great significance to clarify the relationship between the two. Based on data from 2000, 2010 and 2020, the urbanization level and ecosystem services of the study area were evaluated. The spatial correlation of ecosystem services was analyzed by Moran’s I. A spatial Durbin model (SDM) was selected to fit the regression. The results show that (1) from 2000 to 2020, the ecosystem services in the study area displayed obvious regional characteristics and aggregation characteristics; (2) in plain areas, the indirect effects of economic, population and land urbanization have a greater negative impact, and compared with shallow mountain areas, deep mountain areas are more negatively affected by economic urbanization and land urbanization; and (3) the significant difference in regression results reflects the rationality of using the spatial Durbin model, as in this paper, and proves the scientific nature of regional coordinated development. The research results provide a reference for the future coordinated development of regional economies and environments