scholarly journals Maternal High-Fat Diet Programs for Metabolic Disturbances in Offspring despite Leptin Sensitivity

2012 ◽  
Vol 96 (4) ◽  
pp. 272-284 ◽  
Author(s):  
Ana Maria Volpato ◽  
Alini Schultz ◽  
Eduardo Magalhães-da-Costa ◽  
Marcelo Lima de Gusmão Correia ◽  
Márcia Barbosa Águila ◽  
...  
Keyword(s):  
High Fat Diet ◽  
High Fat ◽  
Metabolic Disturbances ◽  
Leptin Sensitivity

Maternal high fat diet during gestation or suckling alters offspring leptin sensitivity prior to weaning

Appetite ◽  
2011 ◽  
Vol 57 ◽  
pp. S42
Author(s):  
B. Sun ◽  
R.H. Purcell ◽  
E.R. Ewald ◽  
J.Q. Yan ◽  
T.H. Moran ◽  
...  
Keyword(s):  
High Fat Diet ◽  
High Fat ◽  
Leptin Sensitivity

Protective effects of phyllanthin, a lignan from Phyllanthus amarus, against progression of high fat diet induced metabolic disturbances in mice

RSC Advances ◽  
2016 ◽  
Vol 6 (63) ◽  
pp. 58343-58353 ◽  
Author(s):  
Sneha Jagtap ◽  
Pragyanshu Khare ◽  
Priyanka Mangal ◽  
Kanthi Kiran Kondepudi ◽  
Mahendra Bishnoi ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Lipid Peroxidation ◽  
Glucose Metabolism ◽  
High Fat Diet ◽  
Phyllanthus Amarus ◽  
Protective Effects ◽  
Liver Inflammation ◽  
High Fat ◽  
Metabolic Disturbances ◽  
Induced Changes

Phyllanthin delayed the progression of high fat diet induced changes affecting lipid and glucose metabolism such as adiposity, hypertriglyceridemia, fatty liver, inflammation, lipid peroxidation and insulin resistance.

Beneficial effects of tamoxifen on leptin sensitivity in young mice fed a high fat diet: Role of estrogen receptor α and cytokines

Life Sciences ◽  
2020 ◽  
Vol 246 ◽  
pp. 117384
Author(s):  
Zeinab Farhadi ◽  
Mohammad Khaksari ◽  
Hossein Azizian ◽  
Abbas Mortazaeizadeh ◽  
Mohammad Shabani ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
High Fat Diet ◽  
Estrogen Receptor Α ◽  
High Fat ◽  
Beneficial Effects ◽  
Leptin Sensitivity ◽  
Young Mice

scholarly journals Protection Against High-Fat Diet-Induced Obesity in Helz2-Deficient Male Mice Due to Enhanced Expression of Hepatic Leptin Receptor

Endocrinology ◽  
2014 ◽  
Vol 155 (9) ◽  
pp. 3459-3472 ◽  
Author(s):  
Satoshi Yoshino ◽  
Tetsurou Satoh ◽  
Masanobu Yamada ◽  
Koshi Hashimoto ◽  
Takuya Tomaru ◽  
...  
Keyword(s):  
Gene Expression ◽  
Protein Kinase ◽  
High Fat Diet ◽  
Leptin Receptor ◽  
Leptin Resistance ◽  
High Fat ◽  
Leptin Sensitivity ◽  
Amp Activated Protein Kinase ◽  
Central Leptin Resistance ◽  
Deficient Mice

Abstract Obesity arises from impaired energy balance, which is centrally coordinated by leptin through activation of the long form of leptin receptor (Leprb). Obesity causes central leptin resistance. However, whether enhanced peripheral leptin sensitivity could overcome central leptin resistance remains obscure. A peripheral metabolic organ targeted by leptin is the liver, with low Leprb expression. We here show that mice fed a high-fat diet (HFD) and obese patients with hepatosteatosis exhibit increased expression of hepatic helicase with zinc finger 2, a transcriptional coactivator (Helz2), which functions as a transcriptional coregulator of several nuclear receptors, including peroxisome proliferator-activated receptor γ in vitro. To explore the physiological importance of Helz2, we generated Helz2-deficient mice and analyzed their metabolic phenotypes. Helz2-deficient mice showing hyperleptinemia associated with central leptin resistance were protected against HFD-induced obesity and had significantly up-regulated hepatic Leprb expression. Helz2 deficiency and adenovirus-mediated liver-specific exogenous Leprb overexpression in wild-type mice significantly stimulated hepatic AMP-activated protein kinase on HFD, whereas Helz2-deficient db/db mice lacking functional Leprb did not. Fatty acid-β oxidation was increased in Helz2-deficeint hepatocytes, and Helz2-deficient mice revealed increased oxygen consumption and decreased respiratory quotient in calorimetry analyses. The enhanced hepatic AMP-activated protein kinase energy-sensing pathway in Helz2-deficient mice ameliorated hyperlipidemia, hepatosteatosis, and insulin resistance by reducing lipogenic gene expression and stimulating lipid-burning gene expression in the liver. These findings together demonstrate that Helz2 deficiency ameliorates HFD-induced metabolic abnormalities by stimulating endogenous hepatic Leprb expression, despite central leptin resistance. Hepatic HELZ2 might be a novel target molecule for the treatment of obesity with hepatosteatosis.

Serum amyloid A1 levels and amyloid deposition following a high-fat diet challenge in transgenic mice overexpressing hepatic serum amyloid A1

2016 ◽  
Vol 41 (6) ◽  
pp. 640-648 ◽  
Author(s):  
Woo Young Jang ◽  
Jain Jeong ◽  
Seonggon Kim ◽  
Min-cheol Kang ◽  
Yong Hun Sung ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Amyloid Deposition ◽  
Serum Amyloid ◽  
Low Grade ◽  
High Fat ◽  
Metabolic Disturbances ◽  
Amyloid A ◽  
Inflammatory Conditions ◽  
Short Period ◽  
Serum Amyloid A1

Serum amyloid A (SAA) is an acute-phase response protein in the liver, and SAA1 is the major precursor protein involved in amyloid A amyloidosis. This amyloidosis has been reported as a complication in chronic inflammatory conditions such as arthritis, lupus, and Crohn’s disease. Obesity is also associated with chronic, low-grade inflammation and sustained, elevated levels of SAA1. However, the contribution of elevated circulating SAA1 to metabolic disturbances and their complications is unclear. Furthermore, in several recent studies of transgenic (TG) mice overexpressing SAA1 that were fed a high-fat diet (HFD) for a relatively short period, no relationship was found between SAA1 up-regulation and metabolic disturbances. Therefore, we generated TG mice overexpressing SAA1 in the liver, challenged these mice with an HFD, and investigated the influence of elevated SAA1 levels. Sustained, elevated levels of SAA1 were correlated with metabolic parameters and local cytokine expression in the liver following 16 weeks on the HFD. Moreover, prolonged consumption (52 weeks) of the HFD was associated with impaired glucose tolerance and elevated SAA1 levels and resulted in systemic SAA1-derived amyloid deposition in the kidney, liver, and spleen of TG mice. Thus, we concluded that elevated SAA1 levels under long-term HFD exposure result in extensive SAA1-derived amyloid deposits, which may contribute to the complications associated with HFD-induced obesity and metabolic disorders.

scholarly journals n-3 PUFA prevent metabolic disturbances associated with obesity and improve endothelial function in golden Syrian hamsters fed with a high-fat diet

2011 ◽  
Vol 107 (9) ◽  
pp. 1305-1315 ◽  
Author(s):  
Fatima Kasbi Chadli ◽  
Agnès Andre ◽  
Xavier Prieur ◽  
Gervaise Loirand ◽  
Anne Meynier ◽  
...  
Keyword(s):  
Endothelial Function ◽  
Glucose Intolerance ◽  
High Fat Diet ◽  
Regulatory Element ◽  
Control Diet ◽  
Scavenger Receptor ◽  
Hdl Cholesterol ◽  
Control Group ◽  
High Fat ◽  
Metabolic Disturbances

Glucose intolerance and dyslipidaemia are independent risk factors for endothelium dysfunction and CVD. The aim of the present study was to analyse the preventive effect of n-3 PUFA (EPA and DHA) on lipid and carbohydrate disturbances and endothelial dysfunction. Three groups of adult hamsters were studied for 20 weeks: (1) control diet (Control); (2) high-fat diet (HF); (3) high-fat diet enriched with n-3 PUFA (HFn-3) groups. The increase in body weight and fat mass in the HF compared to the Control group (P < 0·05) was not found in the HFn-3 group. Muscle TAG content was similar in the Control and HF groups, but significantly lower in the HFn-3 group (P = 0·008). Glucose tolerance was impaired in the HF compared to the Control group, but this impairment was prevented by n-3 PUFA in the HFn-3 group (P < 0·001). Plasma TAG and cholesterol were higher in the HF group compared to the Control group (P < 0·001), but lower in the HFn-3 group compared to the HF group (P < 0·001). HDL-cholesterol was lower in the HFn-3 group compared to the Control and HF groups (P < 0·0005). Hepatic secretion of TAG was lower in the HFn-3 group compared to the HF group (P < 0·005), but did not differ from the Control group. Hepatic gene expression of sterol regulatory element-binding protein-1c, diacylglycerol O-acyltransferase 2 and stearyl CoA desaturase 1 was lower in the HFn-3 group, whereas carnitine palmitoyl transferase 1 and scavenger receptor class B type 1 expression was higher (P < 0·05). In adipocytes and adipose macrophages, PPARγ and TNFα expression was higher in the HF and HFn-3 groups compared to the Control group. Endothelium relaxation was higher in the HFn-3 (P < 0·001) than in the HF and Control groups, and was correlated with glucose intolerance (P = 0·03) and cholesterol (P = 0·0003). In conclusion, n-3 PUFA prevent some metabolic disturbances induced by high-fat diet and improve endothelial function in hamsters.

scholarly journals Sex and Exposure to Postnatal Chlorpyrifos Influence the Epigenetics of Feeding-Related Genes in a Transgenic APOE Mouse Model: Long-Term Implications on Body Weight after a High-Fat Diet

2020 ◽  
Vol 18 (1) ◽  
pp. 184
Author(s):  
Laia Guardia-Escote ◽  
Jordi Blanco ◽  
Pia Basaure ◽  
Judit Biosca-Brull ◽  
Rikst Nynke Verkaik-Schakel ◽  
...  
Keyword(s):  
Body Weight ◽  
Epigenetic Regulation ◽  
High Fat Diet ◽  
Leptin Receptor ◽  
Metabolic Response ◽  
Apoe Genotype ◽  
The Body ◽  
High Fat ◽  
Metabolic Disturbances ◽  
Developmental Exposure

Developmental exposure to toxicants and diet can interact with an individual’s genetics and produce long-lasting metabolic adaptations. The different isoforms of the apolipoprotein E (APOE) are an important source of variability in metabolic disorders and influence the response to the pesticide chlorpyrifos (CPF). We aimed to study the epigenetic regulation on feeding control genes and the influence of postnatal CPF exposure, APOE genotype, and sex, and how these modifications impact on the metabolic response to a high-fat diet (HFD). Both male and female apoE3- and apoE4-TR mice were exposed to CPF on postnatal days 10–15. The DNA methylation pattern of proopiomelanocortin, neuropeptide Y, leptin receptor, and insulin-like growth factor 2 was studied in the hypothalamus. At adulthood, the mice were given a HFD for eight weeks. The results highlight the importance of sex in the epigenetic regulation and the implication of CPF treatment and APOE genotype. The body weight progression exhibited sex-dimorphic differences, apoE4-TR males being the most susceptible to the effects induced by CPF and HFD. Overall, these results underscore the pivotal role of sex, APOE genotype, and developmental exposure to CPF on subsequent metabolic disturbances later in life and show that sex is a key variable in epigenetic regulation.

scholarly journals Young APPKI NL-G-F/NL-G-F mice display high-fat diet-induced metabolic disturbances and specific disorders associated with brain energy homeostasis.

2021 ◽  
Author(s):  
Wei Wang ◽  
Daisuke Tanokashira ◽  
Megumi Maruyama ◽  
Chiemi Kuroiwa ◽  
Takashi Saito ◽  
...  
Keyword(s):  
Mouse Models ◽  
High Fat Diet ◽  
Early Life ◽  
Energy Homeostasis ◽  
Normal Diet ◽  
Aging Effects ◽  
High Fat ◽  
Metabolic Disturbances ◽  
Increased Risk ◽  
Brain Energy

Aim: Type 2 diabetes mellitus (T2DM) is an increased risk factor for Alzheimer's disease (AD); however, the relationship between the two conditions is controversial. High-fat diet (HFD) causes cognitive impairment with/without Aβ accumulation in middle-aged or aged transgenic (Tg) and knock-in (KI) AD mouse models, except for metabolic disorders, which commonly occur in all mice types. Alternatively, whether HFD in early life impacts energy metabolism and neurological phenotypes in young AD mouse models remains unknown. In the present study, we examined the effects of HFD on young APPKI NL-G-F/NL-G-F mice, one of the novel knock-in (KI)-AD mouse models. Methods: The mice were categorized by diet into two experimental groups, normal diet (ND) and HFD. Four-week-old WT and APPKI NL-G-F/NL-G-F mice were fed ND or HFD for nine weeks. Both types of mice on ND and HFD were examined during young adulthood. Results: HFD causes T2DM-related metabolic disturbances in young WT and APPKI NL-G-F/NL-G-F mice and specific impairment of brain energy homeostasis only in young APPKI NL-G-F/NL-G-F mice. However, HFD-induced metabolic dysfunctions had no impact on behaviors, Aβ levels, and specific IRS1 modifications in both young APPKI NL-G-F/NL-G-F mice and young WT mice. Conclusion: HFD in early life is effective in causing metabolic disturbances in young WT and APPKI NL-G-F/NL-G-F mice but is ineffective in inducing neurological disorders in young mice, which suggests that the aging effects along with long-term HFD cause neurological alterations.

Sign in / Sign up

Export Citation Format

Share Document