Maternal perinatal calorie restriction temporally regulates the hepatic autophagy and redox status in male rat

Devarajan, Asokan; Rajasekaran, Namakkal S.; Valburg, Claire; Ganapathy, Ekambaram; Bindra, Snehal; Freije, William A.

doi:10.1016/j.freeradbiomed.2018.09.029

Cited by 23 publications

(31 citation statements)

References 31 publications

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“…A study demonstrated that autophagy may serve a role in NAFLD formation in offspring ( 32 ). Lipophagy (a type of selective autophagy) mainly involves the selective degradation of cytoplasmic lipid droplets, so hepatocyte autophagy is currently considered a defense mechanism in the prevention of NAFLD ( 33 ).…”

Section: Discussionmentioning

confidence: 99%

Maternal obesity accelerated non‑alcoholic fatty liver disease in offspring mice by reducing autophagy

et al. 2021

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Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease characterized by an excessive accumulation of triacylglycerol in the liver. Autophagy is a lysosome-dependent degradation product recovery process, which widely occurs in eukaryotic cells, responsible for the vital maintenance of cellular energy balance. Previously published studies have demonstrated that autophagy is closely related to NAFLD occurrence and maternal obesity increases the susceptibility of offspring to non-alcoholic fatty liver disease, however, the underlying mechanism of this remains unclear. In the present study, NAFLD mouse models (offspring of an obese mother mouse via high-fat feeding) were generated, and the physiological indices of the liver were observed using total cholesterol, triglyceride, high-density lipoprotein and low-density lipoprotein serum assay kits. The morphological changes of the liver were also observed via HE, Masson and oil red O staining. Reverse transcription-quantitative-PCR and western blotting were performed to detect changes of autophagy-related genes in liver or fibrosis marker proteins (α-smooth muscle actin or TGF-β 1 ). Changes in serum inflammatory cytokine IL-6 levels were determined via ELISA. The results of the present study demonstrated that the offspring of an obese mother were more likely to develop NALFD than the offspring of a chow-fed mother, due to their increased association with liver fibrosis. When feeding continued to 17 weeks, the worst cases of NAFLD were observed and the level of autophagy decreased significantly compared with the offspring of a normal weight mouse. In addition, after 17 weeks of feeding, compared with the offspring of a chow-fed mother, the offspring of an obese mouse mother had reduced adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) phosphorylation levels and increased mammalian target of rapamycin (mTOR) phosphorylation levels. These results suggested that a reduced level of AMPK/mTOR mediated autophagy may be of vital importance for the increased susceptibility of offspring to NAFLD caused by maternal obesity. In conclusion, the current study provided a new direction for the treatment of NAFLD in offspring caused by maternal obesity.

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Section: Discussionmentioning

confidence: 99%

Maternal obesity accelerated non‑alcoholic fatty liver disease in offspring mice by reducing autophagy

et al. 2021

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“…Based on CR experimen cytokine, chemokine, and metabolic pathways are significantly regulated by CR the aging process. It is expected that a better understanding of senoinflam mechanisms will provide a basis for the discovery of molecular targets that modulate age-related chronic inflammatory conditions and enable the develop effective interventions to delay aging and prevent the occurrence of aging-assoc ├ Human, Mouse, Rat [255][256][257][258] Lipid accumulation ↑ and mice without SIRT3 genes have decreased HB concentration during fasting [1 are also related to low levels of insulin [213,214], suppressed IGF signaling [215], i [209] and activation of AMPK [215,216] and antioxidant genes [209]. K neuroprotective and lifespan extension effects similar to CR in C. elegans [21 transcription of antioxidant genes, including manganese superoxide dismu FOXO3, both of which exert antioxidant effects [209].…”

Section: Discussionmentioning

confidence: 99%

Anti-Aging Effects of Calorie Restriction (CR) and CR Mimetics Based on the Senoinflammation Concept

et al. 2020

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Chronic inflammation, a pervasive feature of the aging process, is defined by a continuous, multifarious, low-grade inflammatory response. It is a sustained and systemic phenomenon that aggravates aging and can lead to age-related chronic diseases. In recent years, our understanding of age-related chronic inflammation has advanced through a large number of investigations on aging and calorie restriction (CR). A broader view of age-related inflammation is the concept of senoinflammation, which has an outlook beyond the traditional view, as proposed in our previous work. In this review, we discuss the effects of CR on multiple phases of proinflammatory networks and inflammatory signaling pathways to elucidate the basic mechanism underlying aging. Based on studies on senoinflammation and CR, we recognized that senescence-associated secretory phenotype (SASP), which mainly comprises cytokines and chemokines, was significantly increased during aging, whereas it was suppressed during CR. Further, we recognized that cellular metabolic pathways were also dysregulated in aging; however, CR mimetics reversed these effects. These results further support and enhance our understanding of the novel concept of senoinflammation, which is related to the metabolic changes that occur in the aging process. Furthermore, a thorough elucidation of the effect of CR on senoinflammation will reveal key insights and allow possible interventions in aging mechanisms, thus contributing to the development of new therapies focused on improving health and longevity.

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“…These offspring also displayed increased protein levels of complex IV of the electron transport chain, suggesting that ATP availability may be reduced due to accelerated ATP hydrolysis [43]. In a rat model of caloric restriction, a 50% decrease in maternal caloric intake from gestational day 11 through PND 21 (i.e., the point of weaning) resulted in increased lipid peroxidation marker 4hydroxynonenol (4HNE) and decreased glutathione protein levels at three weeks [44]. Adult offspring had unaltered 4HNE and antioxidant levels after switching to a control diet at weaning, suggesting that the caloric restriction itself had caused the oxidative stress [44].…”

Section: Oxidative Stress and Mitochondrial Dysfunctionmentioning

confidence: 99%

“…In a rat model of caloric restriction, a 50% decrease in maternal caloric intake from gestational day 11 through PND 21 (i.e., the point of weaning) resulted in increased lipid peroxidation marker 4hydroxynonenol (4HNE) and decreased glutathione protein levels at three weeks [44]. Adult offspring had unaltered 4HNE and antioxidant levels after switching to a control diet at weaning, suggesting that the caloric restriction itself had caused the oxidative stress [44]. Many studies using the maternal protein restriction (MPR) rat model have also established that catch-up growth may be of greater detriment to hepatic mitochondrial function rather than the original in utero nutritional insult.…”

Section: Oxidative Stress and Mitochondrial Dysfunctionmentioning

confidence: 99%

The Role of Cellular Stress in Intrauterine Growth Restriction and Postnatal Dysmetabolism

Oke¹,

Hardy²

2021

Preprint

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Disruption of the in utero environment can have dire consequences on fetal growth and development. Intrauterine growth restriction (IUGR) is a pathological condition by which the fetus deviates from its expected growth trajectory, resulting in low birth weight and impaired organ function. The developmental origins of health and disease (DOHaD) postulates that IUGR has lifelong consequences on offspring well-being, as human studies have established an inverse relationship between birth weight and long-term metabolic health. While these trends are apparent in epidemiological data, animal studies have been essential in defining the molecular mechanisms that contribute to this relationship. One such mechanism is cellular stress, a prominent underlying cause of the metabolic syndrome. As such, this review considers the role of oxidative stress, mitochondrial dysfunction, endoplasmic reticulum (ER) stress, and inflammation in the pathogenesis of metabolic disease in IUGR offspring. In addition, we summarize how uncontrolled cellular stress can lead to programmed cell death within the metabolic organs of IUGR offspring.

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Maternal perinatal calorie restriction temporally regulates the hepatic autophagy and redox status in male rat

Cited by 23 publications

References 31 publications

Maternal obesity accelerated non‑alcoholic fatty liver disease in offspring mice by reducing autophagy

Maternal obesity accelerated non‑alcoholic fatty liver disease in offspring mice by reducing autophagy

Anti-Aging Effects of Calorie Restriction (CR) and CR Mimetics Based on the Senoinflammation Concept

The Role of Cellular Stress in Intrauterine Growth Restriction and Postnatal Dysmetabolism

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