scholarly journals High-Fat Programming of Hyperglycemia, Hyperinsulinemia, Insulin Resistance, Hyperleptinemia, and Altered Islet Architecture in 3-Month-Old Wistar Rats

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Marlon E. Cerf ◽  
Charna S. Chapman ◽  
Johan Louw
Keyword(s):  
Cell Proliferation ◽  
Acinar Cell ◽  
High Fat Diet ◽  
Alpha Cell ◽  
Postnatal Life ◽  
Fetal Life ◽  
High Fat ◽  
Cell Hyperplasia ◽  
Adult Rats ◽  
Ki 67

High-fat programming, by exposure to a high-saturated-fat diet in utero and/or during lactation, compromises beta-cell development and function in neonatal and weanling offspring. Therefore, high-fat programming effects were investigated on metabolism and islet architecture in young adult rats. Three-month-old male and female Wistar rat offspring were studied: HFG (maintained on a high-fat diet throughout fetal life), HFP (high-fat diet maintenance from birth to 3 months), and HFGP (high-fat diet maintenance throughout fetal and postnatal life). Control rats were maintained on a standard laboratory diet. Pancreata were double immunolabeled for insulin and glucagon to assess islet morphology and with Ki-67 to determine islet and acinar cell proliferation. HFP and HFGP males were heavier, hyperleptinemic, and hyperinsulinemic. Hyperglycemia presented in HFP males, HFP females, and HFGP males. HFGP males and HFP females were insulin resistant. HFP males displayed beta- and alpha-cell hyperplasia with alpha-cell hypertrophy evident in HFP females. Acinar cell proliferation rates were increased in HFP males. Postnatal high-fat programming induced the most diabetogenic phenotype with high-fat maintenance throughout fetal and postnatal life resulting in a severely obese phenotype. Fetal and postnatal nutrition shapes offspring health outcomes.

scholarly journals Effects of metformin on compensatory pancreatic β-cell hyperplasia in mice fed a high-fat diet

2017 ◽  
Vol 313 (3) ◽  
pp. E367-E380 ◽  
Author(s):  
Kazuki Tajima ◽  
Jun Shirakawa ◽  
Tomoko Okuyama ◽  
Mayu Kyohara ◽  
Shunsuke Yamazaki ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Cell Proliferation ◽  
High Fat Diet ◽  
Cell Mass ◽  
Mammalian Target Of Rapamycin ◽  
High Fat ◽  
Β Cells ◽  
Β Cell ◽  
Pancreatic Β Cells ◽  
Cell Hyperplasia

Metformin has been widely used for the treatment of type 2 diabetes. However, the effect of metformin on pancreatic β-cells remains controversial. In this study, we investigated the impacts of treatment with metformin on pancreatic β-cells in a mouse model fed a high-fat diet (HFD), which triggers adaptive β-cell replication. An 8-wk treatment with metformin improved insulin resistance and suppressed the compensatory β-cell hyperplasia induced by HFD-feeding. In contrast, the increment in β-cell mass arising from 60 wk of HFD feeding was similar in mice treated with and those treated without metformin. Interestingly, metformin suppressed β-cell proliferation induced by 1 wk of HFD feeding without any changes in insulin resistance. Metformin directly suppressed glucose-induced β-cell proliferation in islets and INS-1 cells in accordance with a reduction in mammalian target of rapamycin phosphorylation. Taken together, metformin suppressed HFD-induced β-cell proliferation independent of the improvement of insulin resistance, partly via direct actions.

Programming by Methyl Donor Deficiency during Pregnancy and Lactation Produces Cardiomyopathy in Adult Rats Subjected to High Fat Diet

2021 ◽  
pp. 2100065
Author(s):  
Zhen Li ◽  
Viola J. Kosgei ◽  
Anais Bison ◽  
Jean‐Marc Alberto ◽  
Remi Umoret ◽  
...  
Keyword(s):  
High Fat Diet ◽  
High Fat ◽  
Adult Rats ◽  
Methyl Donor ◽  
Pregnancy And Lactation

scholarly journals High-Fat Diet Induced Gut Microbiota Alterations Associating With Ghrelin/Jak2/Stat3 Up-Regulation to Promote Benign Prostatic Hyperplasia Development

2021 ◽  
Vol 9 ◽  
Author(s):  
Meng Gu ◽  
Chong Liu ◽  
TianYe Yang ◽  
Ming Zhan ◽  
Zhikang Cai ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Benign Prostatic Hyperplasia ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Prostatic Hyperplasia ◽  
Prostate Tissue ◽  
High Fat ◽  
Ghrelin Receptor

The role of high-fat diet (HFD) induced gut microbiota alteration and Ghrelin as well as their correlation in benign prostatic hyperplasia (BPH) were explored in our study. The gut microbiota was analyzed by 16s rRNA sequencing. Ghrelin levels in serum, along with Ghrelin and Ghrelin receptor in prostate tissue of mice and patients with BPH were measured. The effect of Ghrelin on cell proliferation, apoptosis, and induction of BPH in mice was explored. Our results indicated that BPH mice have the highest ratio of Firmicutes and Bacteroidetes induced by HFD, as well as Ghrelin level in serum and prostate tissue was significantly increased compared with control. Elevated Ghrelin content in the serum and prostate tissue of BPH patients was also observed. Ghrelin promotes cell proliferation while inhibiting cell apoptosis of prostate cells. The effect of Ghrelin on enlargement of the prostate was found almost equivalent to that of testosterone propionate (TP) which may be attenuated by Ghrelin receptor antagonist YIL-781. Ghrelin could up-regulate Jak2/pJak2/Stat3/pStat3 expression in vitro and in vivo. Our results suggested that Gut microbiota may associate with Ghrelin which plays an important role in activation of Jak2/Stat3 in BPH development. Gut microbiota and Ghrelin might be pathogenic factors for BPH and could be used as a target for mediation.

scholarly journals Perinatal Exposure to Bisphenol A at Reference Dose Predisposes Offspring to Metabolic Syndrome in Adult Rats on a High-Fat Diet

Endocrinology ◽  
2011 ◽  
Vol 152 (8) ◽  
pp. 3049-3061 ◽  
Author(s):  
Jie Wei ◽  
Yi Lin ◽  
Yuanyuan Li ◽  
Chenjiang Ying ◽  
Jun Chen ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Bisphenol A ◽  
High Fat Diet ◽  
Perinatal Exposure ◽  
High Fat ◽  
Adult Rats ◽  
Reference Dose

Reduced Compensatory β-Cell Proliferation in Nfatc3-Deficient Mice Fed on High-Fat Diet

2019 ◽  
Author(s):  
Li Hu ◽  
Fengli He ◽  
Yan Luo ◽  
Hairong Luo ◽  
Luo Hai ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
High Fat Diet ◽  
Compensatory Growth ◽  
Pancreatic Β Cell ◽  
High Fat ◽  
Β Cell ◽  
Primary Mouse ◽  
Mouse Islets ◽  
And Function

Abstract Background High-fat-diet induces pancreatic β-cell compensatory proliferation, and impairments in pancreatic β-cell proliferation and function can lead to defects in insulin secretion and diabetes. NFATc3 is important for HFD-induced adipose tissue inflammation. But it is unknown whether NFATc3 is required for β cell compensatory growth in mice fed with HFD. Methods NFATc3 mRNA and protein expression levels were quantified by RT-qPCR and Western blotting, respectively, in pancreatic islets of WT mice fed on HFD for 12–20 weeks. Adenoviral-mediated overexpression of NFATc3 were conducted in Min6 cells and cultured primary mouse islets. NFATc3-/- mice and WT control mice were fed with HFD and metabolic and functional parameters were measured. Results We observed that the NFATc3 expression level was reduced in the islets of high-fat-diet (HFD)-fed mice. Adenovirus-mediated overexpression of NFATc3 enhanced glucose-stimulated insulin secretion and β-cell gene expression in cultured primary mouse islets. Nfatc3-/- mice initially developed similar glucose tolerance at 2–4 weeks after HFD feeding than HFD-fed WT mice, but Nfatc3-/- mice developed improved glucose tolerance and insulin sensitivity after 8 weeks of HFD feeding compared to Nfatc3+/+fed with HFD. Furthermore, Nfatc3-/- mice on HFD exhibited decreased β-cell mass and reduced expression of genes important for β-cell proliferation and function compared to Nfatc3+/+mice on HFD. Conclusions The findings suggested that NFATc3 played a role in maintaining the pancreatic β-cell compensatory growth and gene expression in response to obesity.

A jaboticaba extract prevents prostatic damage associated with aging and high-fat diet intake

2020 ◽  
Vol 11 (2) ◽  
pp. 1547-1559 ◽  
Author(s):  
C. A. Lamas ◽  
L. A. Kido ◽  
F. Montico ◽  
C. B. Collares-Buzato ◽  
M. R. Maróstica ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
High Fat Diet ◽  
High Fat ◽  
Lesion Development ◽  
Diet Intake

Jaboticaba extract prevented the prostatic lesion development in aging and/or overweight mice, mainly interfering in cell proliferation, hormonal and angiogenesis pathways.

scholarly journals Effects of high-fat diet exposure during fetal life on type 2 diabetes development in the progeny

2008 ◽  
Vol 49 (9) ◽  
pp. 1936-1945 ◽  
Author(s):  
Donatella Gniuli ◽  
Alessandra Calcagno ◽  
Maria Emiliana Caristo ◽  
Alessandra Mancuso ◽  
Veronica Macchi ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
High Fat Diet ◽  
Fetal Life ◽  
High Fat ◽  
Diabetes Development ◽  
Diet Exposure

scholarly journals Maternal High-Fat Diet and Offspring Expression Levels of Vitamin K–Dependent Proteins

Endocrinology ◽  
2014 ◽  
Vol 155 (12) ◽  
pp. 4749-4761 ◽  
Author(s):  
S. A. Lanham ◽  
F. R. Cagampang ◽  
R. O. C. Oreffo
Keyword(s):  
Vitamin K ◽  
High Fat Diet ◽  
Maternal Nutrition ◽  
Vascular Tissue ◽  
Bone Structure ◽  
Female Offspring ◽  
Matrix Gla Protein ◽  
Postnatal Life ◽  
High Fat ◽  
Expression Levels

Studies suggest that bone growth and development and susceptibility to vascular disease in later life are influenced by maternal nutrition during intrauterine and early postnatal life. There is evidence for a role of vitamin K–dependent proteins (VKDPs) including osteocalcin, matrix Gla protein, periostin, and growth-arrest specific– protein 6, in both bone and vascular development. We have examined whether there are alterations in these VKDPs in bone and vascular tissue from offspring of mothers subjected to a nutritional challenge: a high-fat diet during pregnancy and postnatally, using 6-week-old mouse offspring. Bone site–specific and sex-specific differences across femoral and vertebral bone in male and female offspring were observed. Overall a high-fat maternal diet and offspring diet exacerbated the bone changes observed. Sex-specific differences and tissue-specific differences were observed in VKDP levels in aorta tissue from high-fat diet–fed female offspring from high-fat diet–fed mothers displaying increased levels of Gas6 and Ggcx compared with those of female controls. In contrast, differences were seen in VKDP levels in femoral bone of female offspring with lower expression levels of Mgp in offspring of mothers fed a high-fat diet compared with those of controls. We observed a significant correlation in Mgp expression levels within the femur to measures of bone structure of the femur and vertebra, particularly in the male offspring cohort. In summary, the current study has highlighted the importance of maternal nutrition on offspring bone development and the correlation of VKDPs to bone structure.

Increased β-cell Proliferation and β-cell Mass Induced Through High Fat Diet in Mice*

2013 ◽  
Vol 7 (3) ◽  
pp. 244
Author(s):  
Kavin Arasi ◽  
Rockann Mosser ◽  
Maureen Gannon
Keyword(s):  
Cell Proliferation ◽  
High Fat Diet ◽  
Cell Mass ◽  
High Fat ◽  
Β Cell
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