scholarly journals In Utero Nutritional Manipulation Provokes Dysregulated Adipocytokines Production in F1 Offspring in Rats

Scientifica ◽  
2016 ◽  
Vol 2016 ◽  
pp. 1-9
Author(s):  
Mervat Y. Hanafi ◽  
Mohamed I. Saad ◽  
Taha M. Abdelkhalek ◽  
Moustafa M. Saleh ◽  
Maher A. Kamel

Background. Intrauterine environment plays a pivotal role in the origin of fatal diseases such as diabetes. Diabetes and obesity are associated with low-grade inflammatory state and dysregulated adipokines production. This study aims to investigate the effect of maternal obesity and malnutrition on adipokines production (adiponectin, leptin, and TNF-α) in F1 offspring in rats.Materials and Methods. Wistar rats were allocated in groups: F1 offspring of control mothers under control diet (CF1-CD) and under high-fat diet (CF1-HCD), F1 offspring of obese mothers under CD (OF1-CD) and under HCD (OF1-HCD), and F1 offspring of malnourished mothers under CD (MF1-CD) and under HCD (MF1-HCD). Every 5 weeks postnatally, blood samples were obtained for biochemical analysis.Results. At the end of the 30-week follow-up, OF1-HCD and MF1-HCD exhibited hyperinsulinemia, moderate dyslipidemia, insulin resistance, and impaired glucose homeostasis compared to CF1-CD and CF1-HCD. OF1-HCD and MF1-HCD demonstrated low serum levels of adiponectin and high levels of leptin compared to CF1-CD and CF1-HCD. OF1-CD, OF1-HCD, and MF1-HCD had elevated serum levels of TNF-αcompared to CF1-CD and CF1-HCD (p<0.05).Conclusion. Maternal nutritional manipulation predisposes the offspring to development of insulin resistance in their adult life, probably via instigating dysregulated adipokines production.

2019 ◽  
Vol 51 (11) ◽  
pp. 714-722 ◽  
Author(s):  
Durr-e-Shewar Ali ◽  
Mohsin Shah ◽  
Asif Ali ◽  
Muhammad Omar Malik ◽  
Farhat Rehman ◽  
...  

AbstractElevated serum levels of inflammatory mediators in conditions such as PCOS reflect a low-grade chronic inflammation and this has been attributed to be associated with insulin-resistance in PCOS. Therefore, insulin-sensitizing agents are suggested to improve both reproductive as well as metabolic aspects of PCOS. This study aimed to compare the effects of metformin taken alone with that of a combination of metformin and pioglitazone on menstrual cycle, hormonal parameters, insulin resistance, and inflammatory biomarkers in women with PCOS. One hundred and six women with PCOS participated in the study. All subjects were randomized into two-arm intervention groups (Arm 1 and 2). Participants in Arm-1 received metformin (500 mg BD) daily while those in Arm-2 a combination of metformin (500 mg BD) and pioglitazone (15 mg BD) for 12 wks. Serum levels of IL-6 and IL-8 were measured using ELISA whereas insulin resistance was assessed using HOMA-IR. At baseline women with PCOS had significantly elevated circulating concentrations of IL-6 and IL-8. Treatment decreased IL-6 in both the groups, however, only the combination group showed a significant decrease (p=0.005). Serum IL-8 level had a significant decrease after treatment in both groups (p <0.001). HOMA-IR and insulin levels also decreased in both the groups (both p <0.001). Testosterone, FSH, and prolactin significantly decreased in both groups. LH also decreased in both groups, however, the change was significant only in the combination group (p=0.013). Combination of metformin and pioglitazone therapy was more effective as compared to metformin alone in reducing the levels of IL-6 and IL-8 as well as insulin resistance in PCOS.


2005 ◽  
Vol 90 (7) ◽  
pp. 4004-4010 ◽  
Author(s):  
Jeannet Lauenborg ◽  
Elisabeth Mathiesen ◽  
Torben Hansen ◽  
Charlotte Glümer ◽  
Torben Jørgensen ◽  
...  

Abstract Context: Diabetes and obesity, components of the metabolic syndrome, are common characteristics of women with prior gestational diabetes mellitus (GDM). Due to increasing incidence of diabetes and obesity, the metabolic syndrome might comprise a major health problem among these women. Objective: The objective was to estimate the prevalence of the metabolic syndrome by three different criteria [World Health Organization 1999 (WHO), The National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults 2001, and European Group for the Study of Insulin Resistance 2002] among women with previous GDM. Design: We conducted a follow-up study of a Danish cohort of women admitted in 1978–1996 to the Diabetes and Pregnancy Center, Rigshospitalet, Copenhagen University Hospital, with diet-treated GDM. The follow-up took place in 2000–2002 at median 9.8 yr (interquartile range 6.4–17.2) after pregnancy. Results were compared with a control group of 1000 age-matched women from a population-based sample (Inter99). Participants: Four hundred eighty-one women at median age 43 yr (interquartile range 38–48) participated. Main Outcome Measures: The main outcome measures were body mass index (BMI), glucose tolerance, blood pressure, lipid profile, and insulin resistance. Results: Independent of the criteria, the prevalence of the metabolic syndrome was three times higher in the prior GDM group, compared with the control group (e.g. WHO: 38.4 vs. 13.4%, P &lt; 0.0005). Age- and BMI-adjusted odds ratio for having the WHO-defined metabolic syndrome was 3.4 (95% confidence interval 2.5–4.8) for the prior GDM group vs. the control group. Obese women (BMI &gt; 30 kg/m2) with previous GDM had a more than 7-fold increased prevalence of the metabolic syndrome (WHO), compared with normal-weight prior GDM women (BMI &lt; 25 kg/m2). In glucose-tolerant women, the prevalence was doubled in the prior GDM group, compared with control group. Conclusion: The prevalence of the metabolic syndrome was three times as high in women with prior diet-treated GDM, compared with age-matched control subjects.


2020 ◽  
Author(s):  
Carine Teles Sangaleti ◽  
Keyla Yukari Katayama ◽  
Kátia De Angelis ◽  
Tércio Lemos de Moraes ◽  
Amanda Aparecida Araújo ◽  
...  

AbstractBackgroundThe metabolic syndrome (MetS) is an obesity-driven disorder with pandemic proportions and limited treatment options. Oxidative stress, low-grade inflammation and altered autonomic regulation, are important components of MetS pathophysiology. We recently reported that galantamine, an acetylcholinesterase inhibitor and an FDA-approved drug (for Alzheimer’s disease) alleviates the inflammatory state in MetS subjects. Here we examined the effects of galantamine on oxidative stress in parallel with inflammatory and cardio-metabolic parameters in subjects with MetS.MethodsThe effects of galantamine treatment, 8 mg daily for 4 weeks, followed by 16 mg daily for 8 weeks or placebo were studied in randomly assigned subjects with MetS (n=22 per group) of both genders. Oxidative stress, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase activities, lipid and protein peroxidation, and nitrite levels were analyzed before and at the end of the treatment. In addition, plasma cytokine and adipokine levels, insulin resistance (HOMA-IR) and other relevant cardio-metabolic indices were analyzed. Autonomic regulation was also examined by heart rate variability (HRV) before treatment, and at every 4 weeks of treatment.ResultsGalantamine treatment significantly increased antioxidant enzyme activities, including SOD (+1.65 USOD/mg protein, [95% CI 0.39 to 2.92], P=0.004) and CAT (+0.93 nmol/mg, [95% CI 0.34 to 1.51], P=0.011), decreased lipid peroxidation (thiobarbituric acid reactive substances, -5.45 pmol/mg, [95% CI -10.97 to 0.067], P=0.053) and systemic nitrite levels (-0.05 nit/mg protein, [95% CI -0.21 to 0.10], P=0.038) compared with placebo. In addition, galantamine significantly alleviated the inflammatory state and insulin resistance, and decreased the low frequency/high frequency ratio of HRV, following 8 and 12 weeks of drug treatment.ConclusionLow-dose galantamine alleviates oxidative stress, alongside beneficial anti-inflammatory, and metabolic effects, and modulates autonomic regulation in subjects with MetS. These findings are of considerable interest for further studies with galantamine to ameliorate MetS pathophysiology.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A613-A613
Author(s):  
Maria Magar ◽  
John Carmichael

Abstract Background: Acromegaly is known to cause insulin resistance through increased gluconeogenesis and reduction in peripheral glucose use; however, hypoglycemia related to acromegaly has not been reported. Clinical Case: A 58-year old man presented for evaluation of several elevated serum IGF1 levels. The patient had reported years of increased body heat but no changes in his hands or feet and no voice deepening. He recently needed 15 dental crowns due to gaps in his teeth. He also had difficult to manage OSA and weight gain. The patient reported neuroglycopenia after a high glycemic meal or drink, although he was never able to objectively measure any low blood glucoses when they occurred; these symptoms improved but did not resolve despite adhering to a low carbohydrate diet. He also had decreased libido and erectile dysfunction. Exam was significant for coarse facial features. Prior testing revealed several elevated IGF1 serum levels, the last one being 227 ng/mL (54-194). One year prior, OGTT resulted in an initial GH level of 0.1 ng/mL with a decrease to &lt;0.1 ng/mL after two hours. Repeat OGTT had an initial GH of 2.98 ng/mL which paradoxically rose to 12 ng/mL. Fasting BG was 90 mg/dL and peaked at 171 mg/dL. Pituitary MRI showed a 5 mm microadenoma, consistent with acromegaly from a GH secreting adenoma. He underwent a TSSC, and his heat intolerance, low libido, and symptom of hypoglycemia resolved completely. Subsequent IGF1 levels and MRI imaging normalized. Postoperatively OGTT showed a peak GH of 0.23 ng/mL with a peak glucose of 134 mg/dL. There was no paradoxical rise in GH. Discussion: Acromegaly is commonly associated with insulin resistance in ~30% of cases; however, there are no reports of associated neuroglycopenia after a carbohydrate-rich meal or OGTT, which in our patient resolved after successful removal of the pituitary microadenoma. His low glucose symptoms could have been a result of reactive hypoglycemia, which is often seen in patients with diabetes or even prediabetes. However this patient had no history of either. He did not have evidence of any tumors causing hypoglycemia and no gastric surgery to suggest a related etiology (e.g, dumping syndrome or nesidioblastosis). Conversely since GH is normally anabolic and stimulates insulin release, the patient’s elevated GH may have caused an abnormal increase in insulin, leading to his hypoglycemia symptoms. Indeed GIP, which stimulates insulin, is thought to be the cause of the paradoxical rise in GH seen in 30% of acromegaly cases. Remarkably, the patient’s hypoglycemia symptoms disappeared after treatment of the acromegaly, which leads us to consider that excess GH was the culprit.


2017 ◽  
Author(s):  
Raghvendra Mall ◽  
Reda Rawi ◽  
Ehsan Ullah ◽  
Khalid Kunji ◽  
Abdelkrim Khadir ◽  
...  

AbstractBackgroundObesity and its co-morbidities are characterized by a chronic low-grade inflammatory state, uncontrolled expression of metabolic measurements and dis-regulation of various forms of stress response. However, the contribution and correlation of inflammation, metabolism and stress responses to the disease are not fully elucidated. In this paper a cross-sectional case study was conducted on clinical data comprising 117 human male and female subjects with and without type 2 diabetes (T2D). Characteristics such as anthropometric, clinical and bio-chemical measurements were collected.MethodsAssociation of these variables with T2D and BMI were assessed using penalized hierarchical linear and logistic regression. In particular, elastic net, hdi and glinternet were used as regularization models to distinguish between cases and controls. Differential network analysis using closed-form approach was performed to identify pairwise-interaction of variables that influence prediction of the phenotype.ResultsFor the 117 participants, physical variables such as PBF, HDL and TBW had absolute coefficients 0.75, 0.65 and 0.34 using the glinternet approach, biochemical variables such as MIP, ROS and RANTES were identified as determinants of obesity with some interaction between inflammatory markers such as IL4, IL-6, MIP, CSF, Eotaxin and ROS. Diabetes was associated with a significant increase in thiobarbituric acid reactive substances (TBARS) which are considered as an index of endogenous lipid peroxidation and an increase in two inflammatory markers, MIP-1 and RANTES. Furthermore, we obtained 13 pairwise effects. The pairwise effects include pairs from and within physical, clinical and biochemical features, in particular metabolic, inflammatory, and oxidative stress markers.ConclusionsWe showcase that markers of oxidative stress (derived from lipid peroxidation) such as MIP-1 and RANTES participate in the pathogenesis of diseases such as diabetes and obesity in the Arab population.


Cells ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 2179
Author(s):  
Maria Kercheva ◽  
Anna M. Gusakova ◽  
Tamara R. Ryabova ◽  
Tatiana E. Suslova ◽  
Julia Kzhyshkowska ◽  
...  

Background: Bone morphogenetic proteins-2 and -4 (BMPs) have been implicated in left ventricular remodeling (LVR) processes such as an inflammation and fibrogenesis. We hypothesized that this knowledge could be translated into clinics. Methods: We studied the dynamics of serum levels of BMPs, its correlation with markers of LVR and with parameters of echocardiography in patients (n = 31) during the six-month follow-up period after myocardial infarction (MI). Results: Elevated serum levels of BMPs decreased by the six-month follow-up period. BMP-2 decreased from the first day after MI, and BMP-4 decreased from the Day 14. The elevated level of BMP-2 at Day 1 was associated with a lower level of troponin I, reperfusion time and better left ventricular ejection fraction (LV EF) at the six-month follow-up. Elevated serum level of BMP-4 at Day 1 was associated with a lower level of a soluble isoform of suppression of tumorigenicity 2 (sST2), age and reperfusion time. An elevated level of BMP-2 at the six-month follow-up was associated with higher levels of BMP-4, high-sensitivity C-reactive protein (hCRP) and sST2. High serum level of BMP-2 correlated with high levels of hCRP and matrix metalloproteinase (MMP)-9 on Day 7. High serum level of BMP-4 correlated with low levels of hCRP, MMP-9 at Day 3, sST2 at Day 1 and with decreased LV EF on Day 7. The findings of multivariate analysis support the involvement of BMP-2 in the development of post-infarction LVR. Conclusions: Our research translates experimental data about the BMPs in the development of adverse LVR into the clinic. Elevated serum levels of BMPs decreased by the end of the six-month period after MI. BMP-2 decreased from the first day and BMP-4 decreased from Day 14. BMP-2 and BMP-4 were associated with the development of LVR. Their correlations with markers of inflammation, degradation of the extracellular matrix, hemodynamic stress and markers of myocardial damage further support our hypothesis. Diagnostic and predictive values of these BMPs at the development of post-infarction LVR in vivo should be investigated further.


2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Camilo P. Martínez-Reyes ◽  
Angélica Y. Gómez-Arauz ◽  
Israel Torres-Castro ◽  
Aarón N. Manjarrez-Reyna ◽  
León F. Palomera ◽  
...  

Experimental evidence in mice suggests a role for interleukin- (IL-) 13 in insulin resistance and low-grade systemic inflammation. However, IL-13 serum levels have not been assessed in subjects with insulin resistance, and associations of IL-13 with parameters of low-grade systemic inflammation are still unknown. Our main goal was to examine the systemic levels of IL-13 in patients with insulin resistance, while also studying the relationship of IL-13 with anthropometric, metabolic, and low-grade systemic inflammatory markers. Ninety-two participants were included in the study and divided into insulin-resistant patients and noninsulin-resistant controls. Blood levels of IL-13, glucose, insulin, triglycerides, cholesterol, tumor necrosis factor-alpha (TNF-α), IL-10, proinflammatory (Mon-CD11c+CD206−), and anti-inflammatory (Mon-CD11c−CD206+) monocytes, as well as anthropometric parameters, were measured in all volunteers. Insulin-resistant patients showed 2.5-fold higher serum levels of IL-13 than controls (P<0.0001) and significantly increased values of TNF-α and Mon-CD11c+CD206−, with concomitant reductions in IL-10 and Mon-CD11c−CD206+. Increased IL-13 was extraordinarily well associated with hyperglycemia (r=0.7362) and hypertriglyceridemia (r=0.7632) but unexpectedly exhibited no significant correlations with TNF-α (r=0.2907), IL-10 (r=−0.3882), Mon-CD11c+CD206− (r=0.2745) or Mon-CD11c−CD206+ (r=−0.3237). This study demonstrates that IL-13 serum levels are elevated in patients with insulin resistance without showing correlation with parameters of low-grade systemic inflammation.


Nutrients ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3451
Author(s):  
Justine Marchix ◽  
Charlène Alain ◽  
Sandrine David-Le Gall ◽  
Luis Alberto Acuña-Amador ◽  
Céline Druart ◽  
...  

Maternal n-6 polyunsaturated fatty acids (PUFA) consumption during gestation and lactation can predispose offspring to the development of metabolic diseases such as obesity later in life. However, the mechanisms underlying the potential programming effect of n-6 PUFA upon offspring physiology are not yet all established. Herein, we investigated the effects of maternal and weaning linoleic acid (LA)-rich diet interactions on gut intestinal and adipose tissue physiology in young (3-month-old) and older (6-month-old) adult offspring. Pregnant rats were fed a control diet (2% LA) or an LA-rich diet (12% LA) during gestation and lactation. At weaning, offspring were either maintained on the maternal diet or fed the other diet for 3 or 6 months. At 3 months of age, the maternal LA-diet favored low-grade inflammation and greater adiposity, while at 6 months of age, offspring intestinal barrier function, adipose tissue physiology and hepatic conjugated linoleic acids were strongly influenced by the weaning diet. The maternal LA-diet impacted offspring cecal microbiota diversity and composition at 3 months of age, but had only few remnant effects upon cecal microbiota composition at 6 months of age. Our study suggests that perinatal exposure to high LA levels induces a differential metabolic response to weaning diet exposure in adult life. This programming effect of a maternal LA-diet may be related to the alteration of offspring gut microbiota.


Sign in / Sign up

Export Citation Format

Share Document