Maternal exposure to high-fat and high-fructose diet evokes hypoadiponectinemia and kidney injury in rat offspring

Yamada-Obara, Nana; Yamagishi, Sho‐ichi; Taguchi, Kensei; Kaida, Yusuke; Yokoro, Miyuki; Nakayama, Yosuke; Ando, Ryoichi; Asanuma, Katsuhiko; Matsui, Takanori; Ueda, Seinosuke; Okuda, Seiya; Fukami, Kei

doi:10.1007/s10157-016-1265-9

Cited by 24 publications

(27 citation statements)

References 31 publications

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“…However, limited data are available at present on the effects of maternal fructose consumption on the BP of adult offspring. Studies listed in Table 1 indicate that consumption of HF alone or as a part of diet by rodent mothers induces programmed hypertension in adult offspring [26,27,28,29,30,31,32,33]. We found that adult offspring of mothers exposed to 60% HF diet during pregnancy and lactation developed hypertension [26], which is consistent with the results of earlier studies involving fructose-fed adult rats [16,19].…”

Section: Effect Of Maternal Fructose Consumption On Programmed Hypsupporting

confidence: 90%

Maternal Fructose Intake Affects Transcriptome Changes and Programmed Hypertension in Offspring in Later Life

2016

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Hypertension originates from early-life insults by so-called “developmental origins of health and disease” (DOHaD). Studies performed in the previous few decades indicate that fructose consumption is associated with an increase in hypertension rate. It is emerging field that tends to unfold the nutrient–gene interactions of maternal high-fructose (HF) intake on the offspring which links renal programming to programmed hypertension. Reprogramming interventions counteract disturbed nutrient–gene interactions induced by maternal HF intake and exert protective effects against developmentally programmed hypertension. Here, we review the key themes on the effect of maternal HF consumption on renal transcriptome changes and programmed hypertension. We have particularly focused on the following areas: metabolic effects of fructose on hypertension and kidney disease; effects of maternal HF consumption on hypertension development in adult offspring; effects of maternal HF consumption on renal transcriptome changes; and application of reprogramming interventions to prevent maternal HF consumption-induced programmed hypertension in animal models. Provision of personalized nutrition is still a faraway goal. Therefore, there is an urgent need to understand early-life nutrient–gene interactions and to develop effective reprogramming strategies for treating hypertension and other HF consumption-related diseases.

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Section: Effect Of Maternal Fructose Consumption On Programmed Hypsupporting

confidence: 90%

Maternal Fructose Intake Affects Transcriptome Changes and Programmed Hypertension in Offspring in Later Life

2016

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“…This review will primarily be limited to MetS-related phenotypes induced by HF consumption in early life in rodent animal models, some of which are listed in Table 1 . Despite fructose alone can alter fetal programming to induce numerous features of MetS [17] , [18] , [19] , [23] , [25] , [26] , [28] , [29] , [30] , some animal studies have often used fructose as a part of diet along with salt [20] , [24] or fat [27] .…”

Section: Effects Of Maternal Fructose Consumption On Developmental Prmentioning

confidence: 99%

“… Types of fructose intake Species Phenotypes related to MetS Age at evaluation Ref. 10% w/v fructose in drinking water throughout lactation Male Sprague–Dawley rats Obesity, insulin resistance 8 weeks [23] 10% w/v fructose plus 4% NaCl in drinking water 28 days before conception and throughout gestation and lactation Male Sprague–Dawley rats Hypertension 9 weeks [24] 60% HF diet throughout pregnancy and lactation Male and female Sprague–Dawley rats Hypertension 3 months [14] , [15] , [17] , [19] 60% HF diet throughout pregnancy and lactation Male Sprague–Dawley rats Hypertension, insulin resistance, dyslipidemia 3 months [16] 60% HF diet throughout pregnancy and lactation plus 1% NaCl in drinking water from weaning to 3 months of age Male Sprague–Dawley rats Hypertension 3 months [20] 60% HF diet throughout pregnancy and lactation Male Sprague–Dawley rats Bladder dysfunction 3 months [18] 10% w/v high fructose corn syrup (HFCS-55) in drinking water throughout pregnancy and lactation Male and female Sprague–Dawley rats Adiposity, dyslipidemia 3 months [25] 10% w/v fructose in drinking water throughout gestation Male Sprague–Dawley rats Insulin resistance 3 months [26] 56.7% HF/high-fat diet throughout pregnancy and lactation Male Sprague–Dawley rats Hypertension, hyperglycemia, kidney disease 4 months [27] 60% HF diet throughout pregnancy and lactation Male Sprague–Dawley rats Dyslipidemia, hepatic steatosis 5 months [28] ...…”

Section: Effects Of Maternal Fructose Consumption On Developmental Prmentioning

confidence: 99%

“…However, limited data are available on the effects of maternal HF induced hypertension in adult offspring. Studies listed in Table 1 indicate that consumption of HF alone or as a part of diet by rodent mothers induces programmed hypertension in adult offspring of both sexes [14] , [15] , [16] , [17] , [19] , [24] , [27] , [30] . Several mechanisms have been proposed to interpret HF-induced hypertension, including oxidative stress, NO deficiency, increased sodium absorption, endothelial dysfunction, activation of the renin-angiotensin system (RAS) activation, and sympathetic nervous system stimulation [11] .…”

Section: Effects Of Maternal Fructose Consumption On Developmental Prmentioning

confidence: 99%

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Translational insights on developmental origins of metabolic syndrome: Focus on fructose consumption

Lee

Leu

et al. 2018

Biomedical Journal

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Metabolic syndrome (MetS) is a highly prevalent complex trait despite recent advances in pathophysiology and pharmacological treatment. MetS can begin in early life by so-called the developmental origins of health and disease (DOHaD). The DOHaD concept offers a novel approach to prevent MetS through reprogramming. High fructose (HF) intake has been associated with increased risk of MetS. HF diet becomes one of the most commonly used animal model to induce MetS. This review discusses the maternal HF diet induced programming process and reprogramming strategy to prevent MetS of developmental origin, with an emphasis on: (1) an overview of metabolic effects of fructose consumption on MetS; (2) insight from maternal HF animal models on MetS-related phenotypes; (3) impact of HF consumption induces organ-specific transcriptome changes; and (4) application of reprogramming strategy to prevent maternal HF consumption-induced MetS. Research into the preventions and treatments of MetS that begin early in life will have a lifelong impact and profound savings in disease burden and financial costs.

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“…AdipoR2 is primarily expressed in the liver and weakly expressed in the kidney, and mediates the activation of peroxisome proliferator-activated receptor α ( 5 , 11 – 13 ). Studies have demonstrated that AdipoR1 protects the kidney against inflammatory, fibrotic or oxidative damage through the activation of AMPK ( 14 – 19 ).…”

Section: Introductionmentioning

confidence: 99%

Uric acid upregulates the adiponectin‑adiponectin receptorï¿½1 pathway in renal proximal tubule epithelial cells

Yang

Xiao

et al. 2017

Mol Med Report

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Adiponectin (APN) is a protein hormone that is primarily derived from adipocytes. It can also be secreted by renal cells. Hypoadiponectinemia has been documented in patients with hyperuricemia, however, whether soluble uric acid (SUA) regulates the expression of APN and APN receptor 1 (AdipoR1) in renal proximal tubule epithelial cells (PTECs) remains to be elucidated. The present study investigated the expression of APN and AdipoR1 in cultured PTECs that were exposed to SUA through immunofluorescence and western blot analysis. In addition, Sprague-Dawley rats with oxonic acid-induced hyperuricemia (HUA) with or without febuxostat treatment were employed as an animal model to measure 24 h urine protein, serum creatinine, urea nitrogen, uric acid and homeostasis model assessment of insulin resistance. Renal pathology was evaluated using hematoxylin and eosin and immunohistochemical staining. APN and AdipoR1 expression in the renal cortex were evaluated by western blotting. The results demonstrated that, in PTECs, the expression of APN and AdipoR1 was constant and increased upon SUA exposure. Similar observations were made within the proximal renal tubules of rats, and the oxonic acid-induced increases in APN and AdipoR1 were offset by febuxostat treatment. Furthermore, SUA-treated PTECs exhibited an increase in the expression of NLR family pyrin domain-containing (NLRP) 3, which was dose-dependent. NLRP3 expression was also significantly increased in the renal cortex of HUA rats compared with control and febuxostat-treated rats. In conclusion, SUA enhanced the expression of APN and AdipoR1 in PTECs, which was associated with an increase in NLRP3 expression. The APN-AdipoR1 pathway was demonstrated to have an important role in in vitro and in vivo models of renal proximal tubule inflammatory injury. Therefore, this pathway may be a potential therapy target in urate nephropathy.

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Maternal exposure to high-fat and high-fructose diet evokes hypoadiponectinemia and kidney injury in rat offspring

Abstract: Our present study suggests that exposure to maternal HFF-diet during fetal and early postnatal development induces hypoadiponectinemia in offspring, which might cause renal injury and metabolic derangements later in life.

Cited by 24 publications

References 31 publications

Maternal Fructose Intake Affects Transcriptome Changes and Programmed Hypertension in Offspring in Later Life

Maternal Fructose Intake Affects Transcriptome Changes and Programmed Hypertension in Offspring in Later Life

Translational insights on developmental origins of metabolic syndrome: Focus on fructose consumption

Uric acid upregulates the adiponectin‑adiponectin receptorï¿½1 pathway in renal proximal tubule epithelial cells

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