Caloric restriction improves glucose homeostasis, yet increases cardiometabolic risk in caveolin-1-deficient mice

Mayurasakorn, Korapat; Hasanah, Nurul; Homma, Tomoyuki; Homma, Mika; Rangel, Isis Katayama; Garza, Amanda E; Romero, José R.; Adler, Gail K.; Williams, Gordon H.; Pojoga, Luminita H.

doi:10.1016/j.metabol.2018.01.012

Cited by 14 publications

(9 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…DR can improve glucose homeostasis and ameliorates diabetes mellitus ( 42 ). Metformin, a widely-used medicine for type 2 diabetes, can mimic DR responses in C. elegans ( 16 ).…”

Section: Resultsmentioning

confidence: 99%

“…Insulin/IGF-1-like signaling is one of most studied lifespan-modulating pathways conserved from invertebrates to vertebrates ( 54 ). Reduced plasma insulin observed in dietary-restricted animals is regarded as a biomarker of longevity ( 42 ). Metformin, a drug that can reduce plasma insulin level, can extend lifespan of C. elegans ( 16 ).…”

Section: Discussionmentioning

confidence: 99%

“…DR has protective effects against AD, amyotropic lateral sclerosis, and various cancers ( 57 , 58 ). The progression of tumors can be delayed by DR in rodents while glucose intolerance and the severity of diabetes in mice can be improved by DR ( 34 , 42 ). A variety of age-related pathologies including cataracts, cognitive impairments, and muscle dysfunction can be attenuated by DR ( 38 , 59 , 60 ).…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Selenocysteine mimics the effect of dietary restriction on lifespan via SKN‑1 and retards age‑associated pathophysiological changes in Caenorhabditis�elegans

Kim

Park

2018

Mol Med Report

View full text Add to dashboard Cite

Selenocysteine, a sulfur-containing amino acid, can modulate cellular oxidative stress defense systems by incorporating into anti-oxidant enzymes such as glutathione peroxidase and thioredoxin reductase. Selenocysteine can also prevent cancer, neurodegenerative diseases and cardiovascular diseases. A recent study revealed that dietary supplementation with selenocysteine can increase the resistance of Caenorhabditis elegans to environmental stressors and its lifespan. The objective of the present study was to identify the underlying mechanism involved in the lifespan-extending effect of selenocysteine and the effect of selenocysteine on age-associated pathophysiological changes. Lifespan assays with known long-lived mutants of age-1 (the ortholog of the phosphoinositide 3-kinase), clk-1 (the ortholog of demethoxyubiquinone hydroxylase) and eat-2 (a ligand-gated ion channel subunit) revealed that the effect of selenocysteine on lifespan specifically overlapped with that of the eat-2 mutation, a genetic model of dietary restriction (DR). Selenocysteine mimicked the effect of DR on the bacterial dilution method. It required SKN-1 (the ortholog of mammalian nuclear factor-erythroid-related factor) for lifespan extension. In addition, selenocysteine significantly delayed the paralysis induced by human amyloid-β gene, positively correlated with the incidence of Alzheimer's disease. The effect of selenocysteine on amyloid-β-induced toxicity was dependent on the nuclear localization of DAF-16. Reduced survival caused by high-glucose-diet was recovered by selenocysteine. Selenocysteine also reduced the cellular level of reactive oxygen species known to be increased by high-glucose-diet. The results of the present study suggested that selenocysteine can mimic the effect of DR on lifespan and age-associated pathophysiological alterations, providing scientific evidence for the development of DR mimetics using selenocysteine.

show abstract

“…DR can improve glucose homeostasis and ameliorates diabetes mellitus ( 42 ). Metformin, a widely-used medicine for type 2 diabetes, can mimic DR responses in C. elegans ( 16 ).…”

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Selenocysteine mimics the effect of dietary restriction on lifespan via SKN‑1 and retards age‑associated pathophysiological changes in Caenorhabditis�elegans

Kim

Park

2018

Mol Med Report

View full text Add to dashboard Cite

show abstract

“…We should note that there is no study considering certain diets in lean humans with CAV1 risk alleles. But, a recent study showed that a caloric restriction regimen greatly decreased bodyweight, triglyceride, cholesterol, and insulin resistance in CAV1 knockout mice [39].…”

Section: Discussionmentioning

confidence: 99%

Interactions between Caveolin 1 polymorphism and the Mediterranean and Mediterranean-DASH Intervention for Neurodegenerative Delay diet (MIND) diet on Metabolic dyslipidemia in overweight and obese adult women: a cross-sectional study

Khatibi

Mirzababaei

Shiraseb

et al. 2021

Preprint

View full text Add to dashboard Cite

Objective: A higher incidence of metabolic dyslipidemia (MD) and its association with many diseases attracted considerable attention to its control. Caveolin 1 (CAV1) is a known gene associated with obesity. Today, a novel diet recognized as the Mediterranean and Mediterranean-DASH Intervention for Neurodegenerative Delay diet (MIND( is reported to have a positive effect on overall health. Hence, we aimed to investigate the interactions between CAV1 polymorphism and MIND diet on the MD in overweight and obese patients.Results: Remarkably, there was a significant interaction between the MIND diet and CAV1 rs3807992 for dyslipidemia (β=-0.25±132, P=0.05) in the crude model. Whereby, subjects with dominant alleles had a lower risk of dyslipidemia and risk allele carriers with higher adherence to MIND diet may exhibit the lower dyslipidemia.This study presented the CAV1 gene as a possible genetic marker in recognizing people at higher risks for metabolic diseases. It also indicated that using the MIND diet may help in improving dyslipidemia through providing a probable interaction with CAV1 rs3807992 polymorphism.

show abstract

“…Based on the available literature, the lack of CAV1 in mice has been associated with poor adaptation to altered metabolic conditions; however, alterations in the levels of glycemia are not always present [ 41 ]. Significant hyperglycemia associated with enhanced gluconeogenesis and elevated lipolysis in CAV1 KO mice has been reported [ 38 , 42 , 43 ]. In our study, HFD induced more significant increases in the insulin levels and adjusted HOMA-IR values of WT compared to CAV1 KO mice ( Figure 2 c); however, elevated levels of insulin and adjusted HOMA-IR values were found in KO mice on CD.…”

Section: Discussionmentioning

confidence: 99%

Loss of Caveolin-1 Is Associated with a Decrease in Beta Cell Death in Mice on a High Fat Diet

Urzúa

Murillo

Castro-Sepúlveda

et al. 2020

IJMS

View full text Add to dashboard Cite

Elevated free fatty acids (FFAs) impair beta cell function and reduce beta cell mass as a consequence of the lipotoxicity that occurs in type 2 diabetes (T2D). We previously reported that the membrane protein caveolin-1 (CAV1) sensitizes to palmitate-induced apoptosis in the beta pancreatic cell line MIN6. Thus, our hypothesis was that CAV1 knock-out (CAV1 KO) mice subjected to a high fat diet (HFD) should suffer less damage to beta cells than wild type (WT) mice. Here, we evaluated the in vivo response of beta cells in the pancreatic islets of 8-week-old C57Bl/6J CAV1 KO mice subjected to a control diet (CD, 14% kcal fat) or a HFD (60% kcal fat) for 12 weeks. We observed that CAV1 KO mice were resistant to weight gain when on HFD, although they had high serum cholesterol and FFA levels, impaired glucose tolerance and were insulin resistant. Some of these alterations were also observed in mice on CD. Interestingly, KO mice fed with HFD showed an adaptive response of the pancreatic beta cells and exhibited a significant decrease in beta cell apoptosis in their islets compared to WT mice. These in vivo results suggest that although the CAV1 KO mice are metabolically unhealthy, they adapt better to a HFD than WT mice. To shed light on the possible signaling pathway(s) involved, MIN6 murine beta cells expressing (MIN6 CAV) or not expressing (MIN6 Mock) CAV1 were incubated with the saturated fatty acid palmitate in the presence of mitogen-activated protein kinase inhibitors. Western blot analysis revealed that CAV1 enhanced palmitate-induced JNK, p38 and ERK phosphorylation in MIN6 CAV1 cells. Moreover, all the MAPK inhibitors partially restored MIN6 viability, but the effect was most notable with the ERK inhibitor. In conclusion, our results suggest that CAV1 KO mice adapted better to a HFD despite their altered metabolic state and that this may at least in part be due to reduced beta cell damage. Moreover, they indicate that the ability of CAV1 to increase sensitivity to FFAs may be mediated by MAPK and particularly ERK activation.

show abstract

Caloric restriction improves glucose homeostasis, yet increases cardiometabolic risk in caveolin-1-deficient mice

Cited by 14 publications

References 46 publications

Selenocysteine mimics the effect of dietary restriction on lifespan via SKN‑1 and retards age‑associated pathophysiological changes in Caenorhabditis�elegans

Selenocysteine mimics the effect of dietary restriction on lifespan via SKN‑1 and retards age‑associated pathophysiological changes in Caenorhabditis�elegans

Interactions between Caveolin 1 polymorphism and the Mediterranean and Mediterranean-DASH Intervention for Neurodegenerative Delay diet (MIND) diet on Metabolic dyslipidemia in overweight and obese adult women: a cross-sectional study

Loss of Caveolin-1 Is Associated with a Decrease in Beta Cell Death in Mice on a High Fat Diet

Contact Info

Product

Resources

About