scholarly journals The conflicting effects of maternal nutrient restriction and early-life obesity on renal health

2011 ◽  
Vol 70 (2) ◽  
pp. 268-275 ◽  
Author(s):  
H. P. Fainberg ◽  
H. Budge ◽  
M. E. Symonds
Keyword(s):  
Early Life ◽  
Animal Studies ◽  
Structural Changes ◽  
Maternal Nutrition ◽  
Renal Diseases ◽  
Low Grade ◽  
Adaptive Responses ◽  
Chronic Inflammatory Response ◽  
Cellular Apoptosis ◽  
Juvenile Obesity

Epidemiological and animal studies have demonstrated that early-life nutrition alters the metabolic responses and generates structural changes in complex tissues, such as the kidneys, which may lead to a reduction in the offspring lifespan. Independently, obesity induces a spontaneous low-grade chronic inflammatory response by modulating several of the major metabolic pathways that ultimately compromise long-term renal health. However, the combined effects of maternal nutrition and early-life obesity in the development of renal diseases are far from conclusive. Previous results, using the ovine model, demonstrated that the combination of a reduction in fetal nutrition and juvenile obesity induced a series of adaptations associated with severe metabolic syndrome in the heart and adipose tissue. Surprisingly, exposure to an obesogenic environment in the kidney of those offspring produced an apparent reduction in glomerulosclerosis in relation to age- and weight-matched controls. However, this reduction in cellular apoptosis was accompanied by a rise in glomerular filtration rate and blood pressure of equal intensity when compared with obese controls. The intention of this review is to explain the adaptive responses observed in this model, based on insights into the mechanism of renal fetal programming, and their potential interactions with some of the metabolic changes produced by obesity.

scholarly journals Ageing, Age-Related Cardiovascular Risk and the Beneficial Role of Natural Components Intake

2021 ◽  
Vol 23 (1) ◽  
pp. 183
Author(s):  
Jacek Rysz ◽  
Beata Franczyk ◽  
Magdalena Rysz-Górzyńska ◽  
Anna Gluba-Brzózka
Keyword(s):  
Animal Studies ◽  
Heart Valves ◽  
Structural Changes ◽  
Cardiac Conduction ◽  
Low Grade ◽  
Dna Mutations ◽  
Age Related ◽  
Low Grade Inflammation ◽  
Natural Way

Ageing, in a natural way, leads to the gradual worsening of the functional capacity of all systems and, eventually, to death. This process is strongly associated with higher metabolic and oxidative stress, low-grade inflammation, accumulation of DNA mutations and increased levels of related damage. Detrimental changes that accumulate in body cells and tissues with time raise the vulnerability to environmental challenges and enhance the risk of major chronic diseases and mortality. There are several theses concerning the mechanisms of ageing: genetic, free radical telomerase, mitochondrial decline, metabolic damage, cellular senescence, neuroendocrine theory, Hay-flick limit and membrane theories, cellular death as well as the accumulation of toxic and non-toxic garbage. Moreover, ageing is associated with structural changes within the myocardium, cardiac conduction system, the endocardium as well as the vasculature. With time, the cardiac structures lose elasticity, and fibrotic changes occur in the heart valves. Ageing is also associated with a higher risk of atherosclerosis. The results of studies suggest that some natural compounds may slow down this process and protect against age-related diseases. Animal studies imply that some of them may prolong the lifespan; however, this trend is not so obvious in humans.

W04.137 Low grade inflammation in juvenile obesity and type I diabetes associated with preatherosclerosis

2004 ◽  
Vol 5 (1) ◽  
pp. 31
Author(s):  
H. Hubmann ◽  
S. Pilz ◽  
M. Borkenstein ◽  
W. März ◽  
L. Stroedter ◽  
...  
Keyword(s):  
Type I Diabetes ◽  
Low Grade ◽  
Type I ◽  
Juvenile Obesity ◽  
Low Grade Inflammation

scholarly journals Therapeutic Effects of Hydrogen in Animal Models of Parkinson's Disease

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Kyota Fujita ◽  
Yusaku Nakabeppu ◽  
Mami Noda
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Animal Models ◽  
Animal Studies ◽  
Clinical Symptoms ◽  
Therapeutic Effects ◽  
Therapeutic Approaches ◽  
Cellular Apoptosis ◽  
6 Hydroxydopamine

Since the first description of Parkinson's disease (PD) nearly two centuries ago, a number of studies have revealed the clinical symptoms, pathology, and therapeutic approaches to overcome this intractable neurodegenerative disease. 1-methy-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 6-hydroxydopamine (6-OHDA) are neurotoxins which produce Parkinsonian pathology. From the animal studies using these neurotoxins, it has become well established that oxidative stress is a primary cause of, and essential for, cellular apoptosis in dopaminergic neurons. Here, we describe the mechanism whereby oxidative stress evokes irreversible cell death, and propose a novel therapeutic strategy for PD using molecular hydrogen. Hydrogen has an ability to reduce oxidative damage and ameliorate the loss of nigrostriatal dopaminergic neuronal pathway in two experimental animal models. Thus, it is strongly suggested that hydrogen might provide a great advantage to prevent or minimize the onset and progression of PD.

scholarly journals Type 1 Diabetic Neuropathy and C-peptide

2004 ◽  
Vol 5 (1) ◽  
pp. 65-77 ◽  
Author(s):  
Anders A. F. Sima ◽  
Weixian Zhang ◽  
George Grunberger
Keyword(s):  
Clinical Trials ◽  
Animal Studies ◽  
Large Scale ◽  
Structural Changes ◽  
Diabetic Complication ◽  
Diabetic Patients ◽  
C Peptide ◽  
Beneficial Effects ◽  
Regulatory Effects

The most common microvascular diabetic complication, diabetic peripheral polyneuropathy (DPN), affects type 1 diabetic patients more often and more severely. In recent decades, it has become increasingly clear that perpetuating pathogenetic mechanisms, molecular, functional, and structural changes and ultimately the clinical expression of DPN differ between the two major types of diabetes. Impaired insulin/C-peptide action has emerged as a crucial factor to account for the disproportionate burden affecting type 1 patients. C-peptide was long believed to be biologically inactive. However, it has now been shown to have a number of insulin-like glucoseindependent effects. Preclinical studies have demonstrated dose-dependent effects onNa+,K+-ATPase activity, endothelial nitric oxide synthase (eNOS), and endoneurial blood flow. Furthermore, it has regulatory effects on neurotrophic factors and molecules pivotal to the integrity of the nodal and paranodal apparatus and modulatory effects on apoptotic phenomena affecting the diabetic nervous system. In animal studies, C-peptide improves nerve conduction abnormalities, prevents nodal degenerative changes, characteristic of type 1 DPN, promotes nerve fiber regeneration, and prevents apoptosis of central and peripheral nerve cell constituents. Limited clinical trials have confirmed the beneficial effects of C-peptide on autonomic and somatic nerve function in patients with type 1 DPN. Therefore, evidence accumulates that replacement of C-peptide in type 1 diabetes prevents and even improves DPN. Large-scale food and drug administration (FDA)-approved clinical trials are necessary to make this natural substance available to the globally increasing type 1 diabetic population.

EXTH-46. MRS BASED BIOMARKERS OF IDH1 MUTANT GLIOMA RESPONSE TO THE IDH INHIBITOR BAY-1436032

2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi173-vi173
Author(s):  
Donghyun Hong ◽  
Noriaki Minami ◽  
Céline Taglang ◽  
Georgios Batsios ◽  
Anne Marie Gillespie ◽  
...  
Keyword(s):  
Animal Models ◽  
Animal Studies ◽  
Response To Treatment ◽  
Resonance Spectroscopy ◽  
Low Grade ◽  
Isocitrate Dehydrogenase 1 ◽  
1H Mrs ◽  
Hyperpolarized 13C ◽  
13C Mrs ◽  
Mutant Idh1

Abstract Gliomas are the most prevalent type of brain tumor in the central nervous system. Mutations in the cytosolic enzyme isocitrate dehydrogenase 1 (IDH1) are a common feature of primary low-grade gliomas, catalyzing the conversion of α-ketoglutarate (αKG) to the oncometabolite 2-hydroxyglutarate (2HG), and mutant IDH1 is a therapeutic target for these tumors. Several mutant IDH inhibitors are currently in clinical trials, nonetheless, complementary non-invasive early biomarkers to assess drug delivery and potential therapeutic response are still needed. The goal of this study was therefore to determine the potential of 1H and hyperpolarized 13C magnetic resonance spectroscopy (MRS)-based biomarkers as indicators of mutant IDH1 low-grade glioma response to treatment with the clinically-relevant IDH1 inhibitor BAY-1436032 in cells and animal models. Immortalized human astrocytes engineered to express mutant IDH1 were treated with 500nM (IC50 value) of BAY-1436032 and BT257 tumors implanted in rats were treated with 150mg/kg of BAY-1436032. To assess steady-state metabolite levels, 1H MRS spectra were acquired on a 500 MHz MRS cancer for cells and a 3 T scanner for animal studies. To assess metabolic fluxes, we used hyperpolarized 13C MRS and probed the fate of hyperpolarized [1-13C]αKG. 1H MRS showed a significant decrease in 2HG as well as a significant increase in glutamate (Glu) and phosphocholine (PCh) following BAY-1436032 treatment in both cell and animal models compared to controls. Furthermore, hyperpolarized 13C MRS showed that hyperpolarized 2HG production from hyperpolarized [1-13C]αKG was decreased and hyperpolarized glutamate production from hyperpolarized [1-13C]αKG was increased in the BAY-1436032 treated groups compared to controls. These findings are consistent with our previous study, which investigated the MRS-detectable consequences of two other mutant IDH inhibitors: AG120 and AG881. Collectively, our work identifies translatable MRS-based metabolic biomarkers of mutant IDH1 inhibition.

scholarly journals The Infant Gut Microbiota and Risk of Asthma: The Effect of Maternal Nutrition during Pregnancy and Lactation

2020 ◽  
Vol 8 (8) ◽  
pp. 1119 ◽  
Author(s):  
Naser A. Alsharairi
Keyword(s):  
Gut Microbiota ◽  
Early Life ◽  
Nutrient Intake ◽  
Maternal Nutrition ◽  
Current Knowledge ◽  
Increased Risk ◽  
Dietary Nutrient ◽  
Pregnancy And Lactation ◽  
Gut Microbiota Composition

Research has amply demonstrated that early life dysbiosis of the gut microbiota influences the propensity to develop asthma. The influence of maternal nutrition on infant gut microbiota is therefore of growing interest. However, a handful of prospective studies have examined the role of maternal dietary patterns during pregnancy in influencing the infant gut microbiota but did not assess whether this resulted in an increased risk of asthma later in life. The mechanisms involved in the process are also, thus far, poorly documented. There have also been few studies examining the effect of maternal dietary nutrient intake during lactation on the milk microbiota, the effect on the infant gut microbiota and, furthermore, the consequences for asthma development remain largely unknown. Therefore, the specific aim of this mini review is summarizing the current knowledge regarding the effect of maternal nutrition during pregnancy and lactation on the infant gut microbiota composition, and whether it has implications for asthma development.

scholarly journals Maternal Nutrition and Epigenetics in Early Life

2013 ◽  
Vol 2 (4) ◽  
pp. 216-224 ◽  
Author(s):  
Marie-France Hivert ◽  
Luigi Bouchard ◽  
Paul W. Franks
Keyword(s):  
Early Life ◽  
Maternal Nutrition

scholarly journals Primary cilia mediate early life programming of adiposity through lysosomal regulation in the developing mouse hypothalamus

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Chan Hee Lee ◽  
Do Kyeong Song ◽  
Chae Beom Park ◽  
Jeewon Choi ◽  
Gil Myoung Kang ◽  
...  
Keyword(s):  
Early Life ◽  
Primary Cilia ◽  
Maternal Nutrition ◽  
Hypothalamic Neurons ◽  
Axonal Projections ◽  
Early Life Programming ◽  
Body Weights ◽  
Cilia Formation ◽  
Obesity In Mice ◽  
Underlying Mechanisms

AbstractHypothalamic neurons including proopiomelanocortin (POMC)-producing neurons regulate body weights. The non-motile primary cilium is a critical sensory organelle on the cell surface. An association between ciliary defects and obesity has been suggested, but the underlying mechanisms are not fully understood. Here we show that inhibition of ciliogenesis in POMC-expressing developing hypothalamic neurons, by depleting ciliogenic genes IFT88 and KIF3A, leads to adulthood obesity in mice. In contrast, adult-onset ciliary dysgenesis in POMC neurons causes no significant change in adiposity. In developing POMC neurons, abnormal cilia formation disrupts axonal projections through impaired lysosomal protein degradation. Notably, maternal nutrition and postnatal leptin surge have a profound impact on ciliogenesis in the hypothalamus of neonatal mice; through these effects they critically modulate the organization of hypothalamic feeding circuits. Our findings reveal a mechanism of early life programming of adult adiposity, which is mediated by primary cilia in developing hypothalamic neurons.

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