PeerJ Preprints: Diabetes and Endocrinologyhttps://peerj.com/preprints/index.atom?journal=peerj&subject=3900Diabetes and Endocrinology articles published in PeerJ PreprintsSex Matters in Health and Disease: a review of biological sex differences with an emphasis on gliomahttps://peerj.com/preprints/277162019-05-092019-05-09Susan Christine MasseyPaula WhitmireTatum E DoyleJoseph E IppolitoMaciej M MrugalaLeland S HuPeter CanollAlexander R A AndersonMelissa A WilsonSusan M FitzpatrickMargaret M McCarthyJoshua B RubinKristin R Swanson
Humans are sexually dimorphic, with sex being the most persistent difference among humans over the course of our evolutionary history. Beyond the visible sex differences that can be considered true dimorphisms, there are also sex differences at the molecular and cellular scales. The role of these biological sex differences for human health, while being increasingly recognized, have long been underappreciated and underexplored. Frequently, these differences are only recognized in sex–specific diseases, such as genitourinary diseases and cancers. However, given the evidence for sex differences in the most basic aspects of human biology, including metabolism, cellular composition, and immune activity, these differences could have consequences for the etiology and pathophysiology of a majority of diseases. It is thus essential to consider the extent to which these differences may influence the various mechanisms underlying disease processes, response to treatment, and the maintenance of health in order to better improve patient outcomes. Here we review the evidence for a broad array of biological sex differences in humans and discuss how they may relate to observed sex differences in various diseases, with an emphasis on cancer, specifically glioblastoma. We further propose that mathematical approaches can be useful for exploring the extent to which sex differences affect disease outcomes and accounting for those in the development of therapeutic strategies.
Humans are sexually dimorphic, with sex being the most persistent difference among humans over the course of our evolutionary history. Beyond the visible sex differences that can be considered true dimorphisms, there are also sex differences at the molecular and cellular scales. The role of these biological sex differences for human health, while being increasingly recognized, have long been underappreciated and underexplored. Frequently, these differences are only recognized in sex–specific diseases, such as genitourinary diseases and cancers. However, given the evidence for sex differences in the most basic aspects of human biology, including metabolism, cellular composition, and immune activity, these differences could have consequences for the etiology and pathophysiology of a majority of diseases. It is thus essential to consider the extent to which these differences may influence the various mechanisms underlying disease processes, response to treatment, and the maintenance of health in order to better improve patient outcomes. Here we review the evidence for a broad array of biological sex differences in humans and discuss how they may relate to observed sex differences in various diseases, with an emphasis on cancer, specifically glioblastoma. We further propose that mathematical approaches can be useful for exploring the extent to which sex differences affect disease outcomes and accounting for those in the development of therapeutic strategies.Hydration, arginine vasopressin, and gluco-regulatory health in humans: A critical perspectivehttps://peerj.com/preprints/276252019-04-012019-04-01Harriet A CarrollLewis J James
Gluco-regulatory diseases, such as type 2 diabetes are currently a key public health priority. Public health messages have started to include the addition of water in their dietary guidelines. Such guidelines however are not based on causal evidence pertaining to the health effects of increased water intake, but rather more heavily based upon non-causal or mechanistic data. One line of thinking linking fluid intake and health is that hypohydration induces elevated blood concentrations of arginine vasopressin (AVP). Research in the 1970s and 1980s implicated AVP in gluco-regulation, supported by observational evidence. This important area of research subsequently appeared to stop until this century during which interest in hypertonic saline infusion studies, animal AVP receptor knockout models, dietary and genetic associations, and human interventions manipulating hydration status have resurged. This narrative review briefly describes and critically evaluates the usefulness of the current AVP-gluco-regulatory research. We offer suggestions on how to test the independent gluco-regulatory effects of body mass reductions versus elevated circulating AVP concentrations, such as investigating hydration manipulations using 3,4-Methylenedioxymethamphetamine. Whilst much research is still needed before making firm conclusions, the current evidence suggests that although AVP may only be partially implicated in gluco-regulation; more ecologically valid models using human participants suggests this effect is independent of hydration status. The key implication of this hypothesis if confirmed in future research is that manipulating hydration status to reduce circulating AVP concentrations may not be an effective method to improve gluco-regulatory health.
Gluco-regulatory diseases, such as type 2 diabetes are currently a key public health priority. Public health messages have started to include the addition of water in their dietary guidelines. Such guidelines however are not based on causal evidence pertaining to the health effects of increased water intake, but rather more heavily based upon non-causal or mechanistic data. One line of thinking linking fluid intake and health is that hypohydration induces elevated blood concentrations of arginine vasopressin (AVP). Research in the 1970s and 1980s implicated AVP in gluco-regulation, supported by observational evidence. This important area of research subsequently appeared to stop until this century during which interest in hypertonic saline infusion studies, animal AVP receptor knockout models, dietary and genetic associations, and human interventions manipulating hydration status have resurged. This narrative review briefly describes and critically evaluates the usefulness of the current AVP-gluco-regulatory research. We offer suggestions on how to test the independent gluco-regulatory effects of body mass reductions versus elevated circulating AVP concentrations, such as investigating hydration manipulations using 3,4-Methylenedioxymethamphetamine. Whilst much research is still needed before making firm conclusions, the current evidence suggests that although AVP may only be partially implicated in gluco-regulation; more ecologically valid models using human participants suggests this effect is independent of hydration status. The key implication of this hypothesis if confirmed in future research is that manipulating hydration status to reduce circulating AVP concentrations may not be an effective method to improve gluco-regulatory health.Pituitary tissue-specific miR-7a-5p regulates FSH expression in rat anterior adenohypophyseal cellshttps://peerj.com/preprints/275032019-01-262019-01-26Chang-Jiang WangHai-Xiang GuoDong-Xu HanZe-Wen YuYi ZhengHao JiangYan GaoBao YuanJia-Bao Zhang
Follicle-stimulating hormone (FSH), which is synthesized and secreted by the anterior pituitary gland, plays an important role in regulating reproductive processes. In this study, using the TargetScan program, we predicted that miRNAs regulate FSH secretion. Dual-luciferase reporter assays were performed and identified miR-7a-5p. MiR-7a-5p has been reported to regulate diverse cellular functions. However, it is unclear whether miR-7a-5p binds to mRNAs and regulates reproductive functions. Therefore, we constructed a suspension of rat anterior pituitary cells and cultured them under adaptive conditions, transfected miR-7a-5p mimics or inhibitor into the cell suspension and detected expression of the FSHb gene. The results demonstrated that miR-7a-5p downregulated FSHb expression levels, while treatment with miR-7a-5p inhibitors upregulated FSHb expression levels relative to those of negative control groups, as shown by quantitative PCR analysis. The results were confirmed with a subsequent experiment showing that FSH secretion was reduced after treatment with mimics and increased in the inhibitor groups, as shown by ELISA. Our results indicated that miR-7a-5p downregulates FSHb expression levels, resulting in decreased FSH synthesis and secretion, which demonstrates the important role of miRNAs in the regulation of FSH and animal reproduction.
Follicle-stimulating hormone (FSH), which is synthesized and secreted by the anterior pituitary gland, plays an important role in regulating reproductive processes. In this study, using the TargetScan program, we predicted that miRNAs regulate FSH secretion. Dual-luciferase reporter assays were performed and identified miR-7a-5p. MiR-7a-5p has been reported to regulate diverse cellular functions. However, it is unclear whether miR-7a-5p binds to mRNAs and regulates reproductive functions. Therefore, we constructed a suspension of rat anterior pituitary cells and cultured them under adaptive conditions, transfected miR-7a-5p mimics or inhibitor into the cell suspension and detected expression of the FSHb gene. The results demonstrated that miR-7a-5p downregulated FSHb expression levels, while treatment with miR-7a-5p inhibitors upregulated FSHb expression levels relative to those of negative control groups, as shown by quantitative PCR analysis. The results were confirmed with a subsequent experiment showing that FSH secretion was reduced after treatment with mimics and increased in the inhibitor groups, as shown by ELISA. Our results indicated that miR-7a-5p downregulates FSHb expression levels, resulting in decreased FSH synthesis and secretion, which demonstrates the important role of miRNAs in the regulation of FSH and animal reproduction.Genetic effect of Type 2 diabetes to the progression of neurological diseaseshttps://peerj.com/preprints/273232018-11-062018-11-06Md Habibur RahmanSilong PengChen ChenPietro Lio’Mohammad Ali Moni
Neurological diseases (NDs) are progressive disorder often advances with age and comorbidities of Type 2 diabetes (T2D). Epidemiological, clinical and neuropathological evidence advocate that patients with T2D are at an increased risk of getting NDs. However, it is very little known how T2D affects the risk and severity of NDs.
To tackle these problems, we employed a transcriptional analysis of affected tissues using agnostic approaches to identify overlapping cellular functions. In this study, we examined gene expression microarray human datasets along with control and disease-affected individuals. Differentially expressed genes (DEG) were identified for both T2D and NDs that includes Alzheimer Disease (AD), Parkinson Disease (PD), Amyotrophic Lateral Sclerosis (ALS), Epilepsy Disease (ED), Huntington Disease (HD), Cerebral Palsy (CP) and Multiple Sclerosis Disease (MSD).
We have developed genetic association and diseasome network of T2D and NDs based on the neighborhood-based benchmarking and multilayer network topology approaches. Overlapping DEG sets go through protein-protein interaction and gene enrichment using pathway analysis and gene ontology methods, identifying numerous candidate common genes and pathways.
Gene expression analysis platforms have been extensively used to investigate altered pathways and to identify potential biomarkers and drug targets. Finally, we validated our identified biomarkers using the gold benchmark datasets which identified corresponding relations of T2D and NDs. Therapeutic targets aimed at attenuating identified altered pathway could ameliorate neurological dysfunction in a T2D patient.
Neurological diseases (NDs) are progressive disorder often advances with age and comorbidities of Type 2 diabetes (T2D). Epidemiological, clinical and neuropathological evidence advocate that patients with T2D are at an increased risk of getting NDs. However, it is very little known how T2D affects the risk and severity of NDs.To tackle these problems, we employed a transcriptional analysis of affected tissues using agnostic approaches to identify overlapping cellular functions. In this study, we examined gene expression microarray human datasets along with control and disease-affected individuals. Differentially expressed genes (DEG) were identified for both T2D and NDs that includes Alzheimer Disease (AD), Parkinson Disease (PD), Amyotrophic Lateral Sclerosis (ALS), Epilepsy Disease (ED), Huntington Disease (HD), Cerebral Palsy (CP) and Multiple Sclerosis Disease (MSD).We have developed genetic association and diseasome network of T2D and NDs based on the neighborhood-based benchmarking and multilayer network topology approaches. Overlapping DEG sets go through protein-protein interaction and gene enrichment using pathway analysis and gene ontology methods, identifying numerous candidate common genes and pathways.Gene expression analysis platforms have been extensively used to investigate altered pathways and to identify potential biomarkers and drug targets. Finally, we validated our identified biomarkers using the gold benchmark datasets which identified corresponding relations of T2D and NDs. Therapeutic targets aimed at attenuating identified altered pathway could ameliorate neurological dysfunction in a T2D patient.Multifunctional roles of Tropomodulin-3 in regulating actin dynamicshttps://peerj.com/preprints/271722018-09-042018-09-04Justin ParrenoVelia M Fowler
Tropomodulins (Tmods) are proteins that cap the slow growing (pointed) ends of actin filaments (F-actin). The basis for our current understanding of Tmod function comes from studies in cells with relatively stable and highly organized F-actin networks, leading to the view that Tmod capping functions principally to preserve F-actin stability. However, not only is Tmod capping dynamic, but it also can play major roles in regulating diverse cellular processes involving F-actin remodeling. Here, we highlight the multifunctional roles of Tmod with a focus on Tmod3. Like other Tmods, Tmod3 binds tropomyosin (Tpm) and actin, capping pure F-actin at submicromolar and Tpm-coated F-actin at nanomolar concentrations. Unlike other Tmods, Tmod3 can also bind actin monomers and its ability to bind actin is inhibited by phosphorylation of Tmod3 by Akt2. Tmod3 is ubiquitously expressed and present in a diverse array of cytoskeletal structures, including contractile structures such as sarcomere-like units of actomyosin stress fibers and in the F-actin network encompassing adherens junctions. Tmod3 participates in F-actin network remodeling in lamellipodia during cell migration, and in the assembly of specialized F-actin networks during exocytosis. Furthermore, Tmod3 is required for development, regulating F-actin mesh formation during meiosis I of mouse oocytes, erythroblast enucleation in definitive erythropoiesis, and megakaryocyte morphogenesis in the mouse fetal liver. Thus, Tmod3 plays vital roles in dynamic and stable F-actin networks in cell physiology and development, with further research required to delineate the mechanistic details of Tmod3 regulation in the aforementioned processes, or in other yet to be discovered processes.
Tropomodulins (Tmods) are proteins that cap the slow growing (pointed) ends of actin filaments (F-actin). The basis for our current understanding of Tmod function comes from studies in cells with relatively stable and highly organized F-actin networks, leading to the view that Tmod capping functions principally to preserve F-actin stability. However, not only is Tmod capping dynamic, but it also can play major roles in regulating diverse cellular processes involving F-actin remodeling. Here, we highlight the multifunctional roles of Tmod with a focus on Tmod3. Like other Tmods, Tmod3 binds tropomyosin (Tpm) and actin, capping pure F-actin at submicromolar and Tpm-coated F-actin at nanomolar concentrations. Unlike other Tmods, Tmod3 can also bind actin monomers and its ability to bind actin is inhibited by phosphorylation of Tmod3 by Akt2. Tmod3 is ubiquitously expressed and present in a diverse array of cytoskeletal structures, including contractile structures such as sarcomere-like units of actomyosin stress fibers and in the F-actin network encompassing adherens junctions. Tmod3 participates in F-actin network remodeling in lamellipodia during cell migration, and in the assembly of specialized F-actin networks during exocytosis. Furthermore, Tmod3 is required for development, regulating F-actin mesh formation during meiosis I of mouse oocytes, erythroblast enucleation in definitive erythropoiesis, and megakaryocyte morphogenesis in the mouse fetal liver. Thus, Tmod3 plays vital roles in dynamic and stable F-actin networks in cell physiology and development, with further research required to delineate the mechanistic details of Tmod3 regulation in the aforementioned processes, or in other yet to be discovered processes.Type II diabetes may affect stem cell niche resulting in down regulation of glucose transporters and insulin receptors in cellshttps://peerj.com/preprints/270242018-07-062018-07-06Wenfa Ng
Characterized by high blood glucose concentration, resistance of cells to glucose uptake and reduced insulin sensitivity, Type II diabetes is a major health problem afflicting both developing and developed countries in increasing extent as populations around the world increasing adopt high energy diets. Given that, in Type II diabetes, successive generations of various cell types in the body ranging from muscles, tissues, blood, and organs are resistant to glucose uptake and exhibited reduced sensitivity to insulin, the underlying aetiology of Type II diabetes might involve the altered gene expression of stem cells in stem cell niches that adapted to a high glucose diet through an evolutionary conserved mechanism that aimed at homeostasis. Specifically, faced with a high energy and high sugar diet, stem cells in stem cell niches around the body possibly activated an evolutionary conserved mechanism aimed at reducing glucose uptake by cells for reducing weight gain by the body. Thus, successive generations of cells generated from the stem cell niche would exhibit an epigenetically controlled programme of gene expression that exhibited down regulation of genes for glucose transporters and insulin receptors. Such cells would display a phenotype of reduced glucose uptake together with reduced sensitivity to insulin; thereby, resulting in a high blood glucose concentration characteristic of Type II diabetes. The above hypothesis helped explain why high sugar intake by the body could result in impaired sensitivity to insulin and reduced glucose uptake by cells, and more importantly, the widespread nature in which many cell types (principally muscle cells) are affected by a possible epigenetically controlled gene expression programme which hitherto appeared clinically irreversible. Specifically, the most important clinical question for diabetes treatment and care remains the reasons underlying the clinically observed irreversible nature of the disease that progressively, with age and poor glucose control, worsens with complications to many organs of the body such as the eyes, kidneys, cardiovascular system and brain (stroke). Interested readers are invited to expand on the ideas presented in this abstract preprint.
Characterized by high blood glucose concentration, resistance of cells to glucose uptake and reduced insulin sensitivity, Type II diabetes is a major health problem afflicting both developing and developed countries in increasing extent as populations around the world increasing adopt high energy diets. Given that, in Type II diabetes, successive generations of various cell types in the body ranging from muscles, tissues, blood, and organs are resistant to glucose uptake and exhibited reduced sensitivity to insulin, the underlying aetiology of Type II diabetes might involve the altered gene expression of stem cells in stem cell niches that adapted to a high glucose diet through an evolutionary conserved mechanism that aimed at homeostasis. Specifically, faced with a high energy and high sugar diet, stem cells in stem cell niches around the body possibly activated an evolutionary conserved mechanism aimed at reducing glucose uptake by cells for reducing weight gain by the body. Thus, successive generations of cells generated from the stem cell niche would exhibit an epigenetically controlled programme of gene expression that exhibited down regulation of genes for glucose transporters and insulin receptors. Such cells would display a phenotype of reduced glucose uptake together with reduced sensitivity to insulin; thereby, resulting in a high blood glucose concentration characteristic of Type II diabetes. The above hypothesis helped explain why high sugar intake by the body could result in impaired sensitivity to insulin and reduced glucose uptake by cells, and more importantly, the widespread nature in which many cell types (principally muscle cells) are affected by a possible epigenetically controlled gene expression programme which hitherto appeared clinically irreversible. Specifically, the most important clinical question for diabetes treatment and care remains the reasons underlying the clinically observed irreversible nature of the disease that progressively, with age and poor glucose control, worsens with complications to many organs of the body such as the eyes, kidneys, cardiovascular system and brain (stroke). Interested readers are invited to expand on the ideas presented in this abstract preprint.Kill two birds with one stone: making multi-transgenic pre-diabetes mouse models through insulin resistance and pancreatic apoptosis pathogenesishttps://peerj.com/preprints/34372017-11-282017-11-28Siyuan KongJinxue RuanKaiyi ZhangBingjun HuYuzhu ChengYubo ZhangShulin YangKui Li
Background. Type 2 diabetes, a chronic disease to which susceptibility is hereditary, is characterized by insulin resistance accompanied by defective insulin secretion. Mouse models, especially transgenic mice, play an important role in medical research. However, the transgenic mouse models that have been used in diabetes research are involved with single transgenes, focusing on the insulin gene or its mutants. Thus they mainly provide information related to Type 1 diabetes.
Methods. Here, we attempted to focus comprehensively on genes related to pancreatic islet damage, peripheral insulin resistance and related environmental inducing factors by generating single-transgenic mice (CHOP), dual-transgenic mice (hIAPP-CHOP) and triple-transgenic mice (11β-HSD1-hIAPP-CHOP). The latter two types of transgenic animals were induced with high-fat, high-sucrose diets (HFHSD). We evaluated and analyzed the diabetes-related symptoms and the histopathological and immunohistochemical features of the transgenic animals.
Results. Specifically, in the triple-transgene animals, the results of intraperitoneal glucose tolerance tests (IPGTT) began to change 60 days after induction (p<0.001). After 190 days of induction, the body weights (p<0.01) and plasma glucose levels of the animals in the Tg group were higher than those of the animals in the Nc group. After the mice were sacrificed, large amounts of lipid were found deposited in the adipose tissues (p<0.01) and ectopically deposited in the non-adipose tissues (p<0.05 or 0.01) of the animals in the Tg HFHSD group. The weights of the kidneys and hearts of the Tg animals were significantly increased (p<0.01). Serum C-P was decreased due to transgene effects, and insulin levels were increased due to the effects of the high-fat high-sucrose diet in the Tg HFHSD group, indicating that damaged insulin secretion and insulin resistance hyperinsulinemia existed simultaneously in these animals. The serum corticosterone levels of the animals in the Tg group were slightly higher than those of the Nc animals due to the effects of the 11βHSD-1 transgene and obesity. In the Tg HFHSD group, hepatic adipose deposition was more severe and the pancreatic islet area was enlarged under compensation, accompanying apoptosis. In the Tg ControlD group, hepatic adipose deposition was also severe, pancreatic islets were damaged, and their areas were decreased (p<0.05), and apoptosis of pancreatic cells occurred. Taken together, these data show that the transgenes led to early-stage pathological changes characteristic of type 2 diabetes in the triple-transgene HFHSD group. The disease of triple-transgenic mice was more severe than that of dual or single-transgenic mice.
Conclusion. The use of multi-transgenes involved in insulin resistance and pancreatic apoptosis is a better way to generate polygene-related early-stage diabetes models.
Background. Type 2 diabetes, a chronic disease to which susceptibility is hereditary, is characterized by insulin resistance accompanied by defective insulin secretion. Mouse models, especially transgenic mice, play an important role in medical research. However, the transgenic mouse models that have been used in diabetes research are involved with single transgenes, focusing on the insulin gene or its mutants. Thus they mainly provide information related to Type 1 diabetes.Methods. Here, we attempted to focus comprehensively on genes related to pancreatic islet damage, peripheral insulin resistance and related environmental inducing factors by generating single-transgenic mice (CHOP), dual-transgenic mice (hIAPP-CHOP) and triple-transgenic mice (11β-HSD1-hIAPP-CHOP). The latter two types of transgenic animals were induced with high-fat, high-sucrose diets (HFHSD). We evaluated and analyzed the diabetes-related symptoms and the histopathological and immunohistochemical features of the transgenic animals.Results. Specifically, in the triple-transgene animals, the results of intraperitoneal glucose tolerance tests (IPGTT) began to change 60 days after induction (p<0.001). After 190 days of induction, the body weights (p<0.01) and plasma glucose levels of the animals in the Tg group were higher than those of the animals in the Nc group. After the mice were sacrificed, large amounts of lipid were found deposited in the adipose tissues (p<0.01) and ectopically deposited in the non-adipose tissues (p<0.05 or 0.01) of the animals in the Tg HFHSD group. The weights of the kidneys and hearts of the Tg animals were significantly increased (p<0.01). Serum C-P was decreased due to transgene effects, and insulin levels were increased due to the effects of the high-fat high-sucrose diet in the Tg HFHSD group, indicating that damaged insulin secretion and insulin resistance hyperinsulinemia existed simultaneously in these animals. The serum corticosterone levels of the animals in the Tg group were slightly higher than those of the Nc animals due to the effects of the 11βHSD-1 transgene and obesity. In the Tg HFHSD group, hepatic adipose deposition was more severe and the pancreatic islet area was enlarged under compensation, accompanying apoptosis. In the Tg ControlD group, hepatic adipose deposition was also severe, pancreatic islets were damaged, and their areas were decreased (p<0.05), and apoptosis of pancreatic cells occurred. Taken together, these data show that the transgenes led to early-stage pathological changes characteristic of type 2 diabetes in the triple-transgene HFHSD group. The disease of triple-transgenic mice was more severe than that of dual or single-transgenic mice.Conclusion. The use of multi-transgenes involved in insulin resistance and pancreatic apoptosis is a better way to generate polygene-related early-stage diabetes models.Prevalence and temporal trends of overweight and obesity among children and adolescents in Jilin, Northeast China, 2011-2015https://peerj.com/preprints/32072017-08-302017-08-30Yan LiZhijun LiQing SunMengying WangMeng JiangYutong ZhouGuanyu WuYali Qi
Objective: In China, the obesity epidemic is truly national and childhood obesity prevalence has rapidly increased and is close to the developed countries. This study aimed to estimate the prevalence and temporal trends of overweight and obesity among children and adolescents in Jilin City, China (2011-2015). Methods: The data derived from the census on students’ constitution and health in 2011-2015 carried out by the Jilin CDC, Jilin City. 191191 children and adolescents aged 7-18 years were included in the present survey, of which 37549 in 2011 to 41564 in the 2015. The newly developed age- and gender-specific BMI cutoffs by the working group on obesity in China were used to define overweight and obesity in children and adolescents. Results: The mean of BMI (body mass index) was significantly increasing from 20.9 kg/m2 in 2011 to 21.5 kg/m2 in 2015 in all subjects. Overweight and Obesity prevalence of total students aged 7-18 years had a significantly increasing from 2012 to 2015 (P<0.001), from 16.0% and 13.1% to 17.1% and 17.1%. The minimum value of BMI and overweight and obesity prevalence in overall age group all presented in 2012. Boys and girls all showed the significant increase in overweight and obesity prevalence in every age group from 2012 to 2015 and boys higher than girls (P<0.001). Regardless of girls and boys, the most likely of children and adolescents being overweight and obesity had been observed in the youngest age and lowest school grade category. Conclusion: In summary, our results indicate that all the overweight and obesity prevalence among children and adolescents over the past 5 years were higher than the 2010 Chinese National Level and Chinese large coastal cities’ level and a significantly increase from 2011-2015. Obesity epidemic is serious, at least not optimistic among children and adolescents in Jilin, Northeast China.
Objective: In China, the obesity epidemic is truly national and childhood obesity prevalence has rapidly increased and is close to the developed countries. This study aimed to estimate the prevalence and temporal trends of overweight and obesity among children and adolescents in Jilin City, China (2011-2015). Methods: The data derived from the census on students’ constitution and health in 2011-2015 carried out by the Jilin CDC, Jilin City. 191191 children and adolescents aged 7-18 years were included in the present survey, of which 37549 in 2011 to 41564 in the 2015. The newly developed age- and gender-specific BMI cutoffs by the working group on obesity in China were used to define overweight and obesity in children and adolescents. Results: The mean of BMI (body mass index) was significantly increasing from 20.9 kg/m2 in 2011 to 21.5 kg/m2 in 2015 in all subjects. Overweight and Obesity prevalence of total students aged 7-18 years had a significantly increasing from 2012 to 2015 (P<0.001), from 16.0% and 13.1% to 17.1% and 17.1%. The minimum value of BMI and overweight and obesity prevalence in overall age group all presented in 2012. Boys and girls all showed the significant increase in overweight and obesity prevalence in every age group from 2012 to 2015 and boys higher than girls (P<0.001). Regardless of girls and boys, the most likely of children and adolescents being overweight and obesity had been observed in the youngest age and lowest school grade category. Conclusion: In summary, our results indicate that all the overweight and obesity prevalence among children and adolescents over the past 5 years were higher than the 2010 Chinese National Level and Chinese large coastal cities’ level and a significantly increase from 2011-2015. Obesity epidemic is serious, at least not optimistic among children and adolescents in Jilin, Northeast China.Preventive effects of salvia officinalis leaf extract on insulin resistance and inflammation, in high fat diet-induced-obesity mice modelhttps://peerj.com/preprints/30862017-07-142017-07-14Mohamed Raafet Ben KhedherMohamed HammamiJonathan Robert ArchDavid Christopher HislopDominic Anthony EzeEdward Taynton WargentMałgorzata Anna KępczyńskaMohamed Sghaier Zaibi
Background: Salvia officinalis (sage) is a native plant to the Mediterranean region and has been used for a long time in traditional medicine for various diseases. We investigated possible anti-diabetic, anti-inflammatory and anti-obesity effects of sage methanol (MetOH) extract in a nutritional mouse model of obesity, inflammation and insulin resistance, as well as its effects on lipolysis and lipogenesis in 3T3-L1 cells.
Methods: Diet-induced obese (DIO) mice were treated for 5 weeks with sage methanol extract (100 and 400 mg.kg -1 /day. bid), or rosiglitazone (3 mg.kg -1 /day. bid), as a positive control. Energy expenditure, food intake, body weight, fat mass, liver glycogen and lipid content were evaluated. Blood glucose, and plasma levels of insulin, lipids leptin and pro- and anti-inflammatory cytokines were measured throughout the experiment. The effects of sage MetOH extract on lipolysis and lipogenesis were tested in vitro in 3T3-L1 cells.
Results: After two weeks of treatment, the lower dose of sage MetOH extract decreased blood glucose and plasma insulin levels during an oral glucose tolerance test (OGTT). An insulin tolerance test (ITT), performed at day 29 confirmed that sage improved insulin sensitivity. Groups treated with low dose sage and rosiglitazone showed very similar effects on OGTT and ITT. Sage also improved HOMA-IR, triglycerides and NEFA. Treatment with the low dose increased the plasma levels of the anti-inflammatory cytokines IL-2, IL-4 and IL-10 and reduced the plasma level of the pro-inflammatory cytokines IL-12, TNF-α, and KC/GRO. The GC analysis revealed the presence of two PPARs agonist in sage MetOH extract. In vitro, the extract reduced in a dose-related manner the accumulation of lipid droplets; however no effect on lipolysis was observed.
Conclusions: Sage MetOH extract at low dose exhibits similar effects to rosiglitazone. It improves insulin sensitivity, inhibits lipogenesis in adipocytes and reduces inflammation as judged by plasma cytokines. Sage presents an alternative to pharmaceuticals for the treatment of diabetes and associated inflammation.
Background: Salvia officinalis (sage) is a native plant to the Mediterranean region and has been used for a long time in traditional medicine for various diseases. We investigated possible anti-diabetic, anti-inflammatory and anti-obesity effects of sage methanol (MetOH) extract in a nutritional mouse model of obesity, inflammation and insulin resistance, as well as its effects on lipolysis and lipogenesis in 3T3-L1 cells.Methods: Diet-induced obese (DIO) mice were treated for 5 weeks with sage methanol extract (100 and 400 mg.kg -1 /day. bid), or rosiglitazone (3 mg.kg -1 /day. bid), as a positive control. Energy expenditure, food intake, body weight, fat mass, liver glycogen and lipid content were evaluated. Blood glucose, and plasma levels of insulin, lipids leptin and pro- and anti-inflammatory cytokines were measured throughout the experiment. The effects of sage MetOH extract on lipolysis and lipogenesis were tested in vitro in 3T3-L1 cells.Results: After two weeks of treatment, the lower dose of sage MetOH extract decreased blood glucose and plasma insulin levels during an oral glucose tolerance test (OGTT). An insulin tolerance test (ITT), performed at day 29 confirmed that sage improved insulin sensitivity. Groups treated with low dose sage and rosiglitazone showed very similar effects on OGTT and ITT. Sage also improved HOMA-IR, triglycerides and NEFA. Treatment with the low dose increased the plasma levels of the anti-inflammatory cytokines IL-2, IL-4 and IL-10 and reduced the plasma level of the pro-inflammatory cytokines IL-12, TNF-α, and KC/GRO. The GC analysis revealed the presence of two PPARs agonist in sage MetOH extract. In vitro, the extract reduced in a dose-related manner the accumulation of lipid droplets; however no effect on lipolysis was observed.Conclusions: Sage MetOH extract at low dose exhibits similar effects to rosiglitazone. It improves insulin sensitivity, inhibits lipogenesis in adipocytes and reduces inflammation as judged by plasma cytokines. Sage presents an alternative to pharmaceuticals for the treatment of diabetes and associated inflammation.Single phase computed tomography is equivalent to dual phase method for localizing hyperfunctioning parathyroid glands in patients with primary hyperparathyroidism: A retrospective reviewhttps://peerj.com/preprints/30582017-06-292017-06-29Fanny MoronAlfred DelumpaJustin ChettaDanielle GuffeyDavid Dunaway
Objective: This study aims to compare the sensitivity of dual phase (non-contrast and arterial) versus single phase (arterial) CT for detection of hyper-functioning parathyroid glands in patients with primary hyperparathyroidism. Methods: The CT scans of thirty-two patients who have biochemical evidence of primary hyperparathyroidism, pathologically proven parathyroid adenomas, and pre-operative multiphase parathyroid imaging were evaluated retrospectively in order to compare the adequacy of single phase vs. dual phase CT scans for the detection of parathyroid adenomas. Results: The parathyroid adenomas were localized in 83% of cases on single arterial phase CT and 80% of cases on dual phase CT. The specificity for localization of parathyroid tumor was 96% for single phase CT and 97% for dual phase CT. The results were not significantly different (p=0.695). These results are similar to those found in the literature for multiphase CT of 55-94%. Conclusions: Our study supports the use of a single arterial phase CT for the detection of hyperfunctioning parathyroid adenomas. Advances in knowledge: A single arterial phase CT has similar sensitivity for localizing parathyroid adenomas as dual phase CT and significantly reduces radiation dose to the patient.
Objective: This study aims to compare the sensitivity of dual phase (non-contrast and arterial) versus single phase (arterial) CT for detection of hyper-functioning parathyroid glands in patients with primary hyperparathyroidism. Methods: The CT scans of thirty-two patients who have biochemical evidence of primary hyperparathyroidism, pathologically proven parathyroid adenomas, and pre-operative multiphase parathyroid imaging were evaluated retrospectively in order to compare the adequacy of single phase vs. dual phase CT scans for the detection of parathyroid adenomas. Results: The parathyroid adenomas were localized in 83% of cases on single arterial phase CT and 80% of cases on dual phase CT. The specificity for localization of parathyroid tumor was 96% for single phase CT and 97% for dual phase CT. The results were not significantly different (p=0.695). These results are similar to those found in the literature for multiphase CT of 55-94%. Conclusions: Our study supports the use of a single arterial phase CT for the detection of hyperfunctioning parathyroid adenomas. Advances in knowledge: A single arterial phase CT has similar sensitivity for localizing parathyroid adenomas as dual phase CT and significantly reduces radiation dose to the patient.