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1.
FASEB J ; 38(10): e23664, 2024 May 31.
Article in English | MEDLINE | ID: mdl-38775797

ABSTRACT

Adipogenesis, a pivotal cellular process involving the differentiation of mesenchymal stem cells (MSCs) to mature adipocytes, plays a significant role in various physiological functions. Dysregulation of adipogenesis is implicated in conditions such as obesity. However, the complete molecular understanding of adipogenesis remains elusive. This study aimed to uncover the novel role of lamina-associated polypeptide 2 alpha (LAP2α) in human adipose-derived stem cells (hASCs) adipogenesis and its impact on high-fat diet (HFD)-induced obesity and associated metabolic disturbances. LAP2α expression was assessed during the adipogenic differentiation of hASCs using RT-qPCR and western blotting. The functional role of LAP2α in adipogenesis was explored both in vitro and in vivo through loss- and gain-of-function studies. Moreover, mice with HFD-induced obesity received lentivirus injection to assess the effect of LAP2α knockdown on fat accumulation. Molecular mechanisms underlying LAP2α in adipogenic differentiation were investigated using RT-qPCR, Western blotting, immunofluorescence staining, and Oil Red O staining. LAP2α expression was upregulated during hASCs adipogenic differentiation. LAP2α knockdown hindered adipogenesis, while LAP2α overexpression promoted adipogenic differentiation. Notably, LAP2α deficiency resisted HFD-induced obesity, improved glucose intolerance, mitigated insulin resistance, and prevented fatty liver development. Mechanistically, LAP2α knockdown attenuated signal transducer and activator of transcription 3 (STAT3) activation by reducing the protein level of phosphorylated STAT3. A STAT3 activator (Colivelin) counteracted the negative impact of LAP2α deficiency on hASCs adipogenic differentiation. Taken together, our current study established LAP2α as a crucial regulator of hASCs adipogenic differentiation, unveiling a new therapeutic target for obesity prevention.


Subject(s)
Adipogenesis , Diet, High-Fat , Mesenchymal Stem Cells , Obesity , Humans , Diet, High-Fat/adverse effects , Obesity/metabolism , Obesity/genetics , Obesity/etiology , Animals , Mice , Mesenchymal Stem Cells/metabolism , Male , Cell Differentiation , Mice, Inbred C57BL , Adipose Tissue/metabolism , Adipose Tissue/cytology , Adipocytes/metabolism , Cells, Cultured , Gene Knockdown Techniques , STAT3 Transcription Factor/metabolism , STAT3 Transcription Factor/genetics , DNA-Binding Proteins , Membrane Proteins
2.
FASEB J ; 38(9): e23643, 2024 May 15.
Article in English | MEDLINE | ID: mdl-38703030

ABSTRACT

Secreted phospholipase A2s are involved in the development of obesity, type 2 diabetes mellitus (T2DM) and cardiovascular disease, which have become serious and growing health concerns worldwide. Integration of genome-wide association study and gene co-expression networks analysis showed that the secreted phospholipase A2 group XIIA (PLA2G12A) may participate in hepatic lipids metabolism. Nevertheless, the role of PLA2G12A in lipid metabolism and its potential mechanism remain elusive. Here, we used AAV9 vector carrying human PLA2G12A gene to exogenously express hPLA2G12A in the liver of mice. We demonstrated that the overexpression of hPLA2G12A resulted in a significant decrease in serum lipid levels in wild-type mice fed with chow diet or high-fat diet (HFD). Moreover, hPLA2G12A treatment protected against diet-induced obesity and insulin resistance in mice fed a HFD. Notably, we found that hPLA2G12A treatment confers protection against obesity and hyperlipidemia independent of its enzymatic activity, but rather by increasing physical activity and energy expenditure. Furthermore, we demonstrated that hPLA2G12A treatment induced upregulation of ApoC2 and Cd36 and downregulation of Angptl8, which contributed to the increase in clearance of circulating triglycerides and hepatic uptake of fatty acids without affecting hepatic de novo lipogenesis, very low-density lipoprotein secretion, or intestinal lipid absorption. Our study highlights the potential of PLA2G12A gene therapy as a promising approach for treating obesity, insulin resistance and T2DM.


Subject(s)
Diet, High-Fat , Energy Metabolism , Insulin Resistance , Mice, Inbred C57BL , Obesity , Triglycerides , Animals , Obesity/metabolism , Obesity/etiology , Mice , Triglycerides/metabolism , Triglycerides/blood , Male , Diet, High-Fat/adverse effects , Humans , Liver/metabolism , Lipid Metabolism
3.
Adipocyte ; 13(1): 2339418, 2024 Dec.
Article in English | MEDLINE | ID: mdl-38706095

ABSTRACT

A Disintegrin And Metalloproteinase domain-containing protein 10 (ADAM10), is involved in several metabolic and inflammatory pathways. We speculated that ADAM10 plays a modulatory role in adipose tissue inflammation and metabolism. To this end, we studied adipose tissue-specific ADAM10 knock-out mice (aKO). While young, regular chow diet-fed aKO mice showed increased insulin sensitivity, following prolonged (33 weeks) high-fat diet (HFD) exposure, aKO mice developed obesity and insulin resistance. Compared to controls, aKO mice showed less inflammatory adipokine profile despite the significant increase in adiposity. In brown adipose tissue, aKO mice on HFD had changes in CD8+ T cell populations indicating a lesser inflammatory pattern. Following HFD, both aKO and control littermates demonstrated decreased adipose tissue pro-inflammatory macrophages, and increased anti-inflammatory accumulation, without differences between the genotypes. Collectively, our observations indicate that selective deletion of ADAM10 in adipocytes results in a mitigated inflammatory response, leading to increased insulin sensitivity in young mice fed with regular diet. This state of insulin sensitivity, following prolonged HFD, facilitates energy storage resulting in increased fat accumulation which ultimately leads to the development of a phenotype of obesity and insulin resistance. In conclusion, the data indicate that ADAM10 has a modulatory effect of inflammation and whole-body energy metabolism.


Subject(s)
ADAM10 Protein , Adipose Tissue , Diet, High-Fat , Mice, Knockout , Animals , Male , Mice , ADAM10 Protein/metabolism , ADAM10 Protein/genetics , Adipocytes/metabolism , Adipose Tissue/metabolism , Amyloid Precursor Protein Secretases/metabolism , Diet, High-Fat/adverse effects , Inflammation/metabolism , Insulin Resistance , Membrane Proteins/metabolism , Membrane Proteins/genetics , Obesity/metabolism , Obesity/etiology , Phenotype
4.
Int J Mol Sci ; 25(9)2024 May 02.
Article in English | MEDLINE | ID: mdl-38732183

ABSTRACT

The impact of microplastics (MPs) on the metabolic functions of the liver is currently unclear and not completely understood. To investigate the effects of the administration of MPs on the hepatic metabolism of normal and obese mice, alterations in the lipid, glucose (Glu), and amino acid regulation pathways were analyzed in the liver and adipose tissues of C57BL/6Korl (wild type, WT) or C57BL/6-Lepem1hwl/Korl mice (leptin knockout, Lep KO) orally administered polystyrene (PS) MPs for 9 weeks. Significant alterations in the lipid accumulation, adipogenesis, lipogenesis, and lipolysis pathways were detected in the liver tissue of MP-treated WT and Lep KO mice compared to the vehicle-treated group. These alterations in their liver tissues were accompanied by an upregulation of the serum lipid profile, as well as alterations in the adipogenesis, lipogenesis, and lipolysis pathways in the adipose tissues of MP-treated WT and Lep KO mice. Specifically, the level of leptin was increased in the adipose tissues of MP-treated WT mice without any change in their food intake. Also, MP-induced disruptions in the glycogenolysis, Glu transporter type 4 (GLUT4)-5' AMP-activated protein kinase (AMPK) signaling pathway, levels of lipid intermediates, and the insulin resistance of the liver tissues of WT and Lep KO mice were observed. Furthermore, the levels of seven endogenous metabolites were remarkably changed in the serum of WT and Lep KO mice after MP administrations. Finally, the impact of the MP administration observed in both types of mice was further verified in differentiated 3T3-L1 adipocytes and HepG2 cells. Thus, these results suggest that the oral administration of MPs for 9 weeks may be associated with the disruption of lipid, Glu, and amino acid metabolism in the liver tissue of obese WT and Lep KO mice.


Subject(s)
Amino Acids , Glucose , Lipid Metabolism , Liver , Mice, Inbred C57BL , Mice, Knockout , Microplastics , Polystyrenes , Animals , Liver/metabolism , Liver/drug effects , Mice , Glucose/metabolism , Lipid Metabolism/drug effects , Amino Acids/metabolism , Administration, Oral , Leptin/metabolism , Adipose Tissue/metabolism , Adipose Tissue/drug effects , Adipogenesis/drug effects , Male , Lipogenesis/drug effects , Obesity/metabolism , Obesity/etiology , Obesity/genetics , Humans , Lipolysis/drug effects
5.
Sci Rep ; 14(1): 11366, 2024 05 18.
Article in English | MEDLINE | ID: mdl-38762543

ABSTRACT

Placental leptin may impact foetal development. Maternal overnutrition has been linked to increased plasma leptin levels and adverse effects on offspring, whereas choline, an essential nutrient for foetal development, has shown promise in mitigating some negative impacts of maternal obesity. Here, we investigate whether a maternal obesogenic diet alters foetal growth and leptin levels in the foetal stomach, amniotic fluid (AF), and placenta in late gestation and explore the potential modulating effects of maternal choline supplementation. Female rats were fed a control (CD) or a western diet (WD) four weeks before mating and during gestation, half of them supplemented with choline (pregnancy days 11-17). Leptin levels (in foetal stomach, AF, and placenta) and leptin gene expression (in placenta) were assessed on gestation days 20 and 21. At day 20, maternal WD feeding resulted in greater leptin levels in foetal stomach, placenta, and AF. The increased AF leptin levels were associated with a premature increase in foetal weight in both sexes. Maternal choline supplementation partially prevented these alterations, but effects differed in CD dams, causing increased AF leptin levels and greater weight in male foetuses at day 20. Maternal choline supplementation effectively mitigates premature foetal overgrowth induced by an obesogenic diet, potentially linked to increased AF leptin levels. Further research is needed to explore the sex-specific effects.


Subject(s)
Amniotic Fluid , Choline , Dietary Supplements , Leptin , Animals , Female , Leptin/blood , Leptin/metabolism , Pregnancy , Choline/administration & dosage , Amniotic Fluid/metabolism , Rats , Male , Placenta/metabolism , Placenta/drug effects , Fetal Development/drug effects , Obesity/metabolism , Obesity/etiology , Fetal Weight/drug effects , Rats, Sprague-Dawley , Diet, Western/adverse effects
6.
In Vivo ; 38(3): 1152-1161, 2024.
Article in English | MEDLINE | ID: mdl-38688615

ABSTRACT

BACKGROUND/AIM: The global prevalence of type 2 diabetes (T2D) continues to increase, necessitating the need for understanding the causes of its development. The widespread use of high-fructose corn syrup (HFCS) in drinks and diets is suspected to play a role in metabolic disorders. Although many studies have reported on the effects of excessive HFCS and excessive energy intakes in middle-aged individuals, few have focused on energy restriction. This study aimed to investigate the effects of excessive HFCS drink intake under energy restriction on developing T2D in early middle-aged mice. MATERIALS AND METHODS: Early middle-aged mice were divided in HFCS and control groups; they were provided either 10% HFCS water or deionized water ad libitum for 12 weeks, respectively. Total energy intake was controlled using a standard rodent diet. Oral glucose tolerance test (OGTT), insulin tolerance test (ITT), tissue weight measurements, serum parameter analyses, and mRNA expression assessments were performed. RESULTS: No increase in body and adipose tissue weight was observed with excessive HFCS intake under energy restriction. Moreover, serum lipid parameters did not differ from those of controls. However, in the OGTT and ITT, the HFCS group showed higher blood glucose levels than the control group. Moreover, the pancreatic weight and insulin II mRNA expression were reduced. CONCLUSION: The excessive HFCS drink intake under energy restriction did not induce obesity; however, it induced impaired glucose tolerance, indicating its negative effects on the pancreas in early middle-aged mice. When translated in human physiology, our results show that even if one does not become obese, excessive HFCS may affect the overall metabolic mechanism; these effects may vary depending on age.


Subject(s)
Blood Glucose , Glucose Tolerance Test , High Fructose Corn Syrup , Animals , High Fructose Corn Syrup/adverse effects , High Fructose Corn Syrup/administration & dosage , Mice , Male , Diabetes Mellitus, Type 2/chemically induced , Diabetes Mellitus, Type 2/etiology , Diabetes Mellitus, Type 2/metabolism , Energy Intake , Disease Models, Animal , Insulin/blood , Body Weight/drug effects , Insulin Resistance , Obesity/etiology , Obesity/metabolism , Obesity/chemically induced
7.
Int J Mol Sci ; 25(7)2024 Apr 02.
Article in English | MEDLINE | ID: mdl-38612776

ABSTRACT

This study examines the impact of insulin-like growth factor 1 (IGF-1) and insulin-like growth factor 2 (IGF-2) on various aspects of children's health-from the realms of growth and puberty to the nuanced characteristics of metabolic syndrome, diabetes, liver pathology, carcinogenic potential, and cardiovascular disorders. A comprehensive literature review was conducted using PubMed, with a Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) method employing specific keywords related to child health, obesity, and insulin-like growth factors. This study reveals associations between insulin-like growth factor 1 and birth weight, early growth, and adiposity. Moreover, insulin-like growth factors play a pivotal role in regulating bone development and height during childhood, with potential implications for puberty onset. This research uncovers insulin-like growth factor 1 and insulin-like growth factor 2 as potential biomarkers and therapeutic targets for metabolic dysfunction-associated liver disease and hepatocellular carcinoma, and it also highlights the association between insulin-like growth factors (IGFs) and cancer. Additionally, this research explores the impact of insulin-like growth factors on cardiovascular health, noting their role in cardiomyocyte hypertrophy. Insulin-like growth factors play vital roles in human physiology, influencing growth and development from fetal stages to adulthood. The impact of maternal obesity on children's IGF levels is complex, influencing growth and carrying potential metabolic consequences. Imbalances in IGF levels are linked to a range of health conditions (e.g., insulin resistance, glucose intolerance, metabolic syndrome, and diabetes), prompting researchers to seek novel therapies and preventive strategies, offering challenges and opportunities in healthcare.


Subject(s)
Diabetes Mellitus , Metabolic Syndrome , Pregnancy , Child , Female , Humans , Insulin-Like Growth Factor I , Insulin-Like Growth Factor II , Metabolic Syndrome/etiology , Obesity/etiology , Insulin-Like Peptides
8.
Front Endocrinol (Lausanne) ; 15: 1359772, 2024.
Article in English | MEDLINE | ID: mdl-38586455

ABSTRACT

Meal timing emerges as a crucial factor influencing metabolic health that can be explained by the tight interaction between the endogenous circadian clock and metabolic homeostasis. Mistimed food intake, such as delayed or nighttime consumption, leads to desynchronization of the internal circadian clock and is associated with an increased risk for obesity and associated metabolic disturbances such as type 2 diabetes and cardiovascular diseases. Conversely, meal timing aligned with cellular rhythms can optimize the performance of tissues and organs. In this review, we provide an overview of the metabolic effects of meal timing and discuss the underlying mechanisms. Additionally, we explore factors influencing meal timing, including internal determinants such as chronotype and genetics, as well as external influences like social factors, cultural aspects, and work schedules. This review could contribute to defining meal-timing-based recommendations for public health initiatives and developing guidelines for effective lifestyle modifications targeting the prevention and treatment of obesity and associated metabolic diseases. Furthermore, it sheds light on crucial factors that must be considered in the design of future food timing intervention trials.


Subject(s)
Circadian Clocks , Diabetes Mellitus, Type 2 , Humans , Circadian Rhythm , Diabetes Mellitus, Type 2/complications , Obesity/etiology , Meals
9.
Am J Clin Nutr ; 119(4): 990-1006, 2024 Apr.
Article in English | MEDLINE | ID: mdl-38569789

ABSTRACT

BACKGROUND: Consumption of sugar-sweetened beverages (SSBs) has been linked to several adverse health outcomes, thus many countries introduced taxation to reduce it. OBJECTIVES: To summarize national SSB taxation laws and to assess their association with obesity, overweight and diabetes. METHODS: We conducted a systematic scoping review up to January 2022 on PubMed, Web of Science, Embase, and Google Search to identify taxes on SSBs. An interrupted time series analysis (ITSA) was conducted on 17 countries with taxation implemented in 2013 or before to evaluate the level and slope modifications in the rate of change of standardized prevalence rates of overweight, obesity, and diabetes. Random-effects meta-regression was used to assess whether year of entry into force of the law, national income, and tax design affected observed results. RESULTS: We included 76 tax laws issued between 1940 and 2020 by 43 countries, which were heterogeneous in terms of tax design, amount, and taxed products. Among children and adolescents, ITSA showed level or slope reduction for prevalence of overweight and obesity in 5 (Brazil, Samoa, Palau, Panama, Tonga) and 6 (El Salvador, Uruguay, Nauru, Norway, Palau, Tonga) countries out of 17, respectively. No clear pattern of modification of results according to investigated factors emerged from the meta-regression analysis. CONCLUSIONS: Taxation is highly heterogeneous across countries in terms of products and design, which might influence its effectiveness. Our findings provide some evidence regarding a deceleration of the increasing prevalence rates of overweight and obesity among children occurring in some countries following introduction of taxation. PROSPERO registration number: CRD42021233309.


Subject(s)
Diabetes Mellitus , Sugar-Sweetened Beverages , Adolescent , Child , Humans , Overweight/epidemiology , Sugar-Sweetened Beverages/adverse effects , Obesity/epidemiology , Obesity/etiology , Taxes , Beverages/adverse effects
10.
Appetite ; 197: 107329, 2024 Jun 01.
Article in English | MEDLINE | ID: mdl-38561064

ABSTRACT

Consumption of sugar-sweetened beverages (SSB) is considered as an important risk factor for the development of overweight and obesity in populations worldwide, with a particular focus on the risks in the younger parts of the population - children and adolescents. Together with fiscal measures and information tools, innovation-based approaches such as the development of sugar-free or sugar-reduced versions of established beverages and development of new beverage products have been used to reduce this challenge, but the effects of product innovation on sugar intake are not well understood from the literature, as previous studies have largely ignored substitution effects of product innovation in the beverage domain. The objective of the present study was to investigate the potential effectiveness of product innovation as a strategy to affect consumers' intake of energy from sweetened non-alcoholic beverages. Using household panel shopping data from approximately 3000 Danish households over the years 2006-2014, we developed a hedonic pricing approach to estimate the influence of product attributes on consumers' utility, based on observed data for Danish households' purchases of sweet drinks. Overall, the study found that beverages' degree of sweetness positively affected the satiation effect of beverage consumption and in turn made the demand for these beverages less sensitive to e.g. price changes or introduction of competing products, whereas the energy density of the beverages positively affected the demand sensitivity to market changes. Findings like these can be useful for assessing market effects as well as environmental and public health impacts of changes to the market environment.


Subject(s)
Consumer Behavior , Sugar-Sweetened Beverages , Child , Adolescent , Humans , Beverages , Obesity/etiology , Obesity/prevention & control , Overweight , Commerce
11.
PLoS One ; 19(4): e0300705, 2024.
Article in English | MEDLINE | ID: mdl-38603672

ABSTRACT

Obesity is a major independent risk factor for chronic kidney disease and can activate renal oxidative stress injury. Ascorbate and aldarate metabolism is an important carbohydrate metabolic pathway that protects cells from oxidative damage. However the effect of oxidative stress on this pathway is still unclear. Therefore, the primary objective of this study was to investigate the ascorbate and aldarate metabolism pathway in the kidneys of high-fat diet-fed obese mice and determine the effects of oxidative stress. Male C57BL/6J mice were fed on a high-fat diet for 12 weeks to induce obesity. Subsequently, non-targeted metabolomics profiling was used to identify metabolites in the kidney tissues of the obese mice, followed by RNA sequencing using transcriptomic methods. The integrated analysis of metabolomics and transcriptomics revealed the alterations in the ascorbate and aldarate metabolic pathway in the kidneys of these high-fat diet-fed obese mice. The high-fat diet-induced obesity resulted in notable changes, including thinning of the glomerular basement membrane, alterations in podocyte morphology, and an increase in oxidative stress. Metabolomics analysis revealed 649 metabolites in the positive-ion mode, and 470 metabolites in the negative-ion mode. Additionally, 659 differentially expressed genes (DEGs) were identified in the obese mice, of which 34 were upregulated and 625 downregulated. Integrated metabolomics and transcriptomics analyses revealed two DEGs and 13 differential metabolites in the ascorbate and aldarate metabolic pathway. The expression levels of ugt1a9 and ugt2b1 were downregulated, and the ascorbate level in kidney tissue of obese mice was reduced. Thus, renal oxidative stress injury induced by high-fat diet affects metabolic regulation of ascorbate and aldarate metabolism in obese mice. Ascorbate emerged as a potential marker for predicting kidney damage due to high-fat diet-induced obesity.


Subject(s)
Diet, High-Fat , Kidney , Animals , Mice , Male , Diet, High-Fat/adverse effects , Mice, Obese , Mice, Inbred C57BL , Kidney/metabolism , Obesity/etiology , Obesity/metabolism , Metabolomics , Gene Expression Profiling
12.
PLoS One ; 19(4): e0301496, 2024.
Article in English | MEDLINE | ID: mdl-38635745

ABSTRACT

Obesity leads to insulin resistance (IR) and type 2 diabetes. In humans, low levels of the hormone prolactin (PRL) correlate with IR, adipose tissue (AT) dysfunction, and increased prevalence of T2D. In obese rats, PRL treatment promotes insulin sensitivity and reduces visceral AT adipocyte hypertrophy. Here, we tested whether elevating PRL levels with the prokinetic and antipsychotic drug sulpiride, an antagonist of dopamine D2 receptors, improves metabolism in high fat diet (HFD)-induced obese male mice. Sulpiride treatment (30 days) reduced hyperglycemia, IR, and the serum and pancreatic levels of triglycerides in obese mice, reduced visceral and subcutaneous AT adipocyte hypertrophy, normalized markers of visceral AT function (PRL receptor, Glut4, insulin receptor and Hif-1α), and increased glycogen stores in skeletal muscle. However, the effects of sulpiride reducing hyperglycemia were also observed in obese prolactin receptor null mice. We conclude that sulpiride reduces obesity-induced hyperglycemia by mechanisms that are independent of prolactin/prolactin receptor activity. These findings support the therapeutic potential of sulpiride against metabolic dysfunction in obesity.


Subject(s)
Diabetes Mellitus, Type 2 , Hyperglycemia , Insulin Resistance , Humans , Mice , Male , Rats , Animals , Mice, Obese , Dopamine D2 Receptor Antagonists , Prolactin , Receptors, Prolactin , Diabetes Mellitus, Type 2/drug therapy , Sulpiride/pharmacology , Sulpiride/therapeutic use , Obesity/drug therapy , Obesity/etiology , Diet, High-Fat/adverse effects , Hyperglycemia/drug therapy , Hypertrophy , Insulin/metabolism
13.
Zebrafish ; 21(2): 223-230, 2024 Apr.
Article in English | MEDLINE | ID: mdl-38621217

ABSTRACT

Obesity is a public health concern resulting in a variety of health complications, including heart disease and insulin resistance. Estrogens have been associated with a reduced risk of obesity, but this relationship remains incompletely understood. We assessed the role of 17ß-estradiol (E2) in mitigating complications associated with obesity by supplementing E2 in the diets of overfed zebrafish. We report that dietary E2 supplementation protects against weight gain and modulates de novo cholesterol synthesis in a sex-specific manner. Our studies lead us to propose a model in which E2 regulates hmgcr expression independently of unsaturated fat consumption. These data can be used to develop sex-specific treatments for obesity-related health conditions.


Subject(s)
Fats, Unsaturated , Zebrafish , Male , Female , Animals , Zebrafish/metabolism , Fats, Unsaturated/metabolism , Estradiol/pharmacology , Estradiol/metabolism , Estrogens/metabolism , Obesity/etiology , Cholesterol/metabolism , Dietary Supplements
14.
Agri ; 36(2): 106-112, 2024 Apr.
Article in English | MEDLINE | ID: mdl-38558400

ABSTRACT

OBJECTIVES: The aim of this study was to investigate the effect of epidural steroid injections on the menstrual cycle of women and to identify risk factors in those with changes. METHODS: A total of 78 women who had epidural steroid injections between the ages of 18 and 55 years were retrospectively analyzed. The patients were called by phone and asked whether there was any change in their menstrual cycles after the epidural injections. Data including demographic and clinical characteristics, body height and weight, education status, alcohol and smoking habits, comorbidities, number of children, birth control method, history of cesarean section, miscarriage, and abortion were recorded. RESULTS: Changes in the menstrual cycle were seen in five of 12 patients who underwent cervical interlaminar epidural steroid injection, in 27 of 56 patients who underwent lumbar transforaminal epidural steroid injection, in one of two patients who underwent lumbar interlaminar epidural steroid injection, and in three of eight patients who underwent caudal epidural steroid injection. The number of patients with obesity was higher in the patients with changes than those without, indicating a statistically significant difference (41.7% vs. 14.3%, respectively; p=0.007). CONCLUSION: Our study suggests that epidural steroid injections are associated with changes in the menstrual cycle. Obesity is a risk factor for menstrual cycle changes after epidural steroid injections.


Subject(s)
Menstrual Cycle , Steroids , Adolescent , Adult , Female , Humans , Middle Aged , Young Adult , Injections, Epidural/adverse effects , Injections, Epidural/methods , Obesity/etiology , Retrospective Studies , Treatment Outcome
15.
Nutrients ; 16(7)2024 Mar 26.
Article in English | MEDLINE | ID: mdl-38612986

ABSTRACT

High-fat diets (HFDs) have pervaded modern dietary habits, characterized by their excessive saturated fat content and low nutritional value. Epidemiological studies have compellingly linked HFD consumption to obesity and the development of type 2 diabetes mellitus. Moreover, the synergistic interplay of HFD, obesity, and diabetes expedites the aging process and prematurely fosters age-related diseases. However, the underlying mechanisms driving these associations remain enigmatic. One of the most conspicuous hallmarks of aging is the accumulation of highly inflammatory senescent cells, with mounting evidence implicating increased cellular senescence in the pathogenesis of age-related diseases. Our hypothesis posits that HFD consumption amplifies senescence burden across multiple organs. To scrutinize this hypothesis, we subjected mice to a 6-month HFD regimen, assessing senescence biomarker expression in the liver, white adipose tissue, and the brain. Aging is intrinsically linked to impaired cellular stress resilience, driven by dysfunction in Nrf2-mediated cytoprotective pathways that safeguard cells against oxidative stress-induced senescence. To ascertain whether Nrf2-mediated pathways shield against senescence induction in response to HFD consumption, we explored senescence burden in a novel model of aging: Nrf2-deficient (Nrf2+/-) mice, emulating the aging phenotype. Our initial findings unveiled significant Nrf2 dysfunction in Nrf2+/- mice, mirroring aging-related alterations. HFD led to substantial obesity, hyperglycemia, and impaired insulin sensitivity in both Nrf2+/- and Nrf2+/+ mice. In control mice, HFD primarily heightened senescence burden in white adipose tissue, evidenced by increased Cdkn2a senescence biomarker expression. In Nrf2+/- mice, HFD elicited a significant surge in senescence burden across the liver, white adipose tissue, and the brain. We postulate that HFD-induced augmentation of senescence burden may be a pivotal contributor to accelerated organismal aging and the premature onset of age-related diseases.


Subject(s)
Diabetes Mellitus, Type 2 , Resilience, Psychological , Animals , Mice , NF-E2-Related Factor 2/genetics , Diet, High-Fat/adverse effects , Diabetes Mellitus, Type 2/etiology , Cellular Senescence , Aging , Obesity/etiology , Biomarkers
16.
Nutrients ; 16(7)2024 Mar 29.
Article in English | MEDLINE | ID: mdl-38613042

ABSTRACT

Recently, intermittent fasting has gained relevance as a strategy to lose weight and improve health as an alternative to continuous caloric restriction. However, the metabolic impact and the sex-related differences are not fully understood. The study aimed to compare the response to a continuous or intermittent caloric restriction in male and female rats following a previous induction of obesity through a cafeteria diet by assessing changes in body weight, energy intake, metabolic parameters, and gene expression in liver hepatic and adipose tissue. The continuous restriction reduced the energy available by 30% and the intermittent restriction consisted of a 75% energy reduction on two non-consecutive days per week. The interventions reduced body weight and body fat in both sexes, but the loss of WAT in females was more marked in both models of caloric restriction, continuous and intermittent. Both caloric restrictions improved insulin sensitivity, but more markedly in females, which showed a more pronounced decrease in HOMA-IR score and an upregulation of hepatic IRS2 and Sirt1 gene expression that was not observed in males. These findings suggest the fact that females are more sensitive than males to reduced caloric content in the diet.


Subject(s)
Diet , Intermittent Fasting , Female , Male , Animals , Rats , Obesity/etiology , Food , Caloric Restriction
17.
Nutrients ; 16(7)2024 Apr 01.
Article in English | MEDLINE | ID: mdl-38613062

ABSTRACT

The adverse influence of maternal obesity on offspring metabolic health throughout the life-course is a significant public health challenge with few effective interventions. We examined if black bean powder (BBP) supplementation to a high-calorie maternal pregnancy diet or a postnatal offspring diet could offer protection against the metabolic programming of metabolic disease risk in adult offspring. Female Sprague Dawley rats were randomly assigned to one of three diets (n = 10/group) for a 3-week pre-pregnancy period and throughout gestation and lactation: (i) a low-caloric control diet (CON); (ii) a high-caloric obesity-inducing diet (HC); or (iii) the HC diet with 20% black bean powder (HC-BBP). At weaning [postnatal day (PND) 21], one male pup from each dam was weaned onto the CON diet throughout the postnatal period until adulthood (PND120). In addition, a second male from the HC group only was weaned onto the CON diet supplemented with BBP (CON-BBP). Thus, based on the maternal diet exposure and offspring postnatal diet, four experimental adult offspring groups were compared: CON/CON, HC/CON, HC-BPP/CON, and HC/CON-BBP. On PND120, blood was collected for biochemical analysis (e.g., lipids, glycemic control endpoints, etc.), and livers were excised for lipid analysis (triglycerides [TG] and cholesterol) and the mRNA/protein expression of lipid-regulatory targets. Compared with the CON/CON group, adult offspring from the HC/CON group exhibited a higher (p < 0.05) body weight (BW) (682.88 ± 10.67 vs. 628.02 ± 16.61 g) and hepatic TG (29.55 ± 1.31 vs. 22.86 ± 1.85 mmol/g). Although maternal BBP supplementation (HC-BBP/CON) had little influence on metabolic outcomes, the consumption of BBP in the postnatal period (HC/CON-BBP) lowered hepatic TG and cholesterol compared with the other treatment groups. Reduced hepatic TG in the HC/CON-BBP was likely associated with lower postnatal BW gain (vs. HC/CON), lower mRNA and protein expression of hepatic Fasn (vs. HC/CON), and lower serum leptin concentration (vs. CON/CON and HC groups). Our results suggest that the postnatal consumption of a black-bean-powder-supplemented diet may protect male rat offspring against the programming of obesity and dyslipidemia associated with maternal obesity. Future work should investigate the bioactive fraction of BBP responsible for the observed effect.


Subject(s)
Dyslipidemias , Obesity, Maternal , Humans , Pregnancy , Adult , Female , Male , Rats , Animals , Powders , Adult Children , Rats, Sprague-Dawley , Obesity/etiology , Obesity/prevention & control , Dyslipidemias/etiology , Dyslipidemias/prevention & control , Cholesterol , RNA, Messenger , Lipids
18.
Int J Mol Sci ; 25(8)2024 Apr 19.
Article in English | MEDLINE | ID: mdl-38674060

ABSTRACT

Mandarin peel, a main by-product from the processing of citrus juice, has been highlighted for its various bioactivities and functional ingredients. Our previous study proved the inhibitory effects of Celluclast extract from mandarin peel (MPCE) on lipid accumulation and differentiation in 3T3-L1 adipocytes. Therefore, the current study aimed to evaluate the anti-obesity effect of MPCE in high-fat diet (HFD)-induced obese mice. The high-performance liquid chromatography (HPLC) analysis exhibited that narirutin and hesperidin are the main active components of MPCE. Our current results showed that MPCE supplementation decreased adiposity by reducing body and organ weights in HFD-induced obese mice. MPCE also reduced triglyceride (TG), alanine transaminase (ALT), aspartate transaminase (AST), and leptin contents in the serum of HFD-fed mice. Moreover, MPCE significantly inhibited hepatic lipid accumulation by regulating the expression levels of proteins associated with lipid metabolism, including sterol regulatory element-binding protein (SREBP1c), fatty acid synthase (FAS), and acetyl-CoA carboxylase (ACC). Furthermore, MPCE administration significantly inhibited both adipogenesis and lipogenesis, with modulation of energy metabolism by activating 5' adenosine monophosphate-activated protein kinase (AMPK) and lipolytic enzymes such as hormone-sensitive lipase (HSL) in the white adipose tissue (WAT). Altogether, our findings indicate that MPCE improves HFD-induced obesity and can be used as a curative agent in pharmaceuticals and nutraceuticals to alleviate obesity and related disorders.


Subject(s)
Adipogenesis , Citrus , Diet, High-Fat , Disaccharides , Energy Metabolism , Flavanones , Mice, Inbred C57BL , Obesity , Plant Extracts , Animals , Diet, High-Fat/adverse effects , Obesity/metabolism , Obesity/drug therapy , Obesity/etiology , Citrus/chemistry , Mice , Energy Metabolism/drug effects , Plant Extracts/pharmacology , Male , Adipogenesis/drug effects , Lipid Metabolism/drug effects , 3T3-L1 Cells , Anti-Obesity Agents/pharmacology , Liver/metabolism , Liver/drug effects , Lipogenesis/drug effects , Triglycerides/metabolism , Triglycerides/blood
19.
Nutrients ; 16(8)2024 Apr 16.
Article in English | MEDLINE | ID: mdl-38674875

ABSTRACT

The prolonged consumption of a high-fat diet (HFD) leads to abnormal growth of the visceral adipose tissue (VAT), increased macrophage infiltration, and altered secretion of biologically active molecules. This is considered as a precondition for the development of obesity, inflammation, and obesity-related disorders. Therefore, we studied HFD-induced changes in the tissue levels of the inflammatory markers C-reactive protein, serum amyloid-A, and interleukin-4 in healthy male Wistar rats. The animals were first divided at random into two groups subjected to either a standard or a high-fat diet. The initial effect of the diet was evaluated after fourteen weeks. In order to study the diet duration effect, the standard diet was given to twelve animals from the HFD group, while the remaining continued with the HFD for an additional four weeks. Our results showed that the HFD barely affected body mass index, conicity, relative fat mass, and Lee indices, whereas it provoked adipocyte hypertrophy and gradually increased the levels of both the pro- and anti-inflammatory markers. The switch from the high-fat to the standard diet resulted in the comparatively fast restoration of the baseline levels of the studied molecules. Although, the prolonged consumption of an HFD causes adipocyte hypertrophy in healthy male animals, the inflammatory process in VAT is well-coordinated, time-dependent, and reversible.


Subject(s)
C-Reactive Protein , Diet, High-Fat , Inflammation , Intra-Abdominal Fat , Rats, Wistar , Animals , Male , Intra-Abdominal Fat/metabolism , Diet, High-Fat/adverse effects , C-Reactive Protein/metabolism , Rats , Serum Amyloid A Protein/metabolism , Interleukin-4/metabolism , Biomarkers/blood , Adipocytes , Obesity/metabolism , Obesity/etiology
20.
Nutrients ; 16(8)2024 Apr 19.
Article in English | MEDLINE | ID: mdl-38674900

ABSTRACT

We aimed to investigate the associations between maternal intake of folate, vitamin B12, B6, B2, methionine, choline, phosphatidylcholine and betaine during the period surrounding pregnancy and offspring weight outcomes from birth to early adulthood. These associations were examined among 2454 mother-child pairs from the Nurses' Health Study II and Growing Up Today Study. Maternal energy-adjusted nutrient intakes were derived from food frequency questionnaires. Birth weight, body size at age 5 and repeated BMI measurements were considered. Overweight/obesity was defined according to the International Obesity Task Force (<18 years) and World Health Organization guidelines (18+ years). Among other estimands, we report relative risks (RRs) for offspring ever being overweight with corresponding 95% confidence intervals across quintiles of dietary factors, with the lowest quintile as the reference. In multivariate-adjusted models, higher maternal intakes of phosphatidylcholine were associated with a higher risk of offspring ever being overweight (RRQ5vsQ1 = 1.16 [1.01-1.33] p-trend: 0.003). The association was stronger among offspring born to mothers with high red meat intake (high red meat RRQ5vsQ1 = 1.50 [1.14-1.98], p-trend: 0.001; low red meat RRQ5vsQ1 = 1.05 [0.87-1.27], p-trend: 0.46; p-interaction = 0.13). Future studies confirming the association between a higher maternal phosphatidylcholine intake during pregnancy and offspring risk of being overweight or obese are needed.


Subject(s)
Maternal Nutritional Physiological Phenomena , Overweight , Humans , Female , Pregnancy , Prospective Studies , Adult , Overweight/epidemiology , Diet/adverse effects , Risk Factors , Male , Obesity/epidemiology , Obesity/etiology , Child, Preschool , Body Mass Index , Choline/administration & dosage , Phosphatidylcholines , Prenatal Exposure Delayed Effects , Birth Weight
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