Reduced expression of SIRT1 is associated with diminished glucose-induced insulin secretion in islets from calorie-restricted rats

Amaral, Maria Esméria Corezola do; Ueno, Mirian; Oliveira, Camila Aparecida Machado de; Borsonello, Natália C.; Vanzela, Emerielle C.; Ribeiro, Rosane Aparecida; Alves, Patricia Lucio; Barbosa, Helena C.; Carneiro, Everardo M.; Boschero, Antônio Carlos

doi:10.1016/j.jnutbio.2010.04.010

Cited by 22 publications

(18 citation statements)

References 35 publications

(47 reference statements)

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“…In the HC/PF rats, there was a suppression of these programmed effects that resurfaced to full capacity in the HC/PF/AL rats. Interestingly, 60% CR imposed on 8-wkold rodent chow-fed rats for 3 wk resulted in diminished glucose-induced insulin secretion in islets (5). Unlike the HC rats, the rats used in that study were not nutritionally malprogrammed for an altered insulin secretory response.…”

Section: Discussionmentioning

confidence: 92%

Metabolic programming effects initiated in the suckling period predisposing for adult-onset obesity cannot be reversed by calorie restriction

Srinivasan

Mahmood

Patel

2013

American Journal of Physiology-Endocrinology and Metabolism

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Srinivasan M, Mahmood S, Patel MS. Metabolic programming effects initiated in the suckling period predisposing for adult-onset obesity cannot be reversed by calorie restriction. Am J Physiol Endocrinol Metab 304: E486 -E494, 2013. First published December 18, 2012 doi:10.1152/ajpendo.00519.2012.-Neonatal rats reared on high-carbohydrate (HC) milk formula developed chronic hyperinsulinemia and adult-onset obesity due to programming of islets and the hypothalamic energy circuitry. In this study, calorie restriction by pair-feeding was imposed on HC male rats (HC/PF) to normalize food intake similar to that of mother-fed (MF) rats from weaning until postnatal day 140. A group of HC/PF rats was switched over to ad libitum feeding (HC/PF/AL) from days 90 to 140. Pair-feeding reduced body weight gains and serum insulin and leptin levels in HC/PF rats compared with HC rats, but these parameters were restored to HC levels in the HC/PF/AL rats after ad libitum feeding. Interestingly, the heightened insulin secretory response of isolated islets from adult HC/PF and HC/PF/ AL rats to glucose, acetylcholine, and oxymetazoline were not significantly different from the responses of islets from HC rats. Similarly, the expression of neuropeptide Y and proopiomelanocortin in the hypothalamus was not significantly different among HC, HC/PF, and HC/PF/AL rats. Expression of the leptin receptor in the hypothalami from the HC, HC/PF, and HC/ PF/AL rats mirrored that of serum leptin, whereas suppressor of cytokine signaling 3 (Socs3) expression remained high in these three groups. The results indicate that, although calorie restriction resulted in reduction in body weight gain and normalized the serum hormonal pattern, the programed predisposition for the hypersecretory capacity of islets and the hypothalamic hyperphagic response in the HC rats could not be permanently overcome by the pair-feeding imposed on HC rats. obesity; hyperinsulinemia; calorie restriction by pair feeding; metabolic programing; suckling period IN THE PERIOD 2009 35.7% of the adult population in the US was classified as obese (BMI Ͼ30) (8). The presence of obesity significantly augments the risk for the onset of a number of metabolic disorders such as hypertension, adverse lipid concentrations, and type 2 diabetes (20). Epidemiological data and results from animal models indicate that altered nutritional experiences during early periods in life (fetal and suckling) can predispose the offspring for the development of obesity and metabolic diseases in later life via developmental programming effects (7). These early adaptations enable the organism to endure the nutritional stress but are detrimental in the long run.Developmental plasticity initiated during fetal development extends into the immediate postnatal period. For example, it has been shown that pancreatic islets and neurons are not fully mature at birth and that their development is completed in the immediate postnatal (suckling) period (10, 12). Hence, an encounter with an altered nutritional experie...

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Section: Discussionmentioning

confidence: 92%

Metabolic programming effects initiated in the suckling period predisposing for adult-onset obesity cannot be reversed by calorie restriction

Srinivasan

Mahmood

Patel

2013

American Journal of Physiology-Endocrinology and Metabolism

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“…Contrary to the metabolic break provided by SIRT4, SIRT3 exerts an opposing regulatory function on the PDH (177). Accordingly, food withdrawal and calorie restriction are associated with increased expression of hepatic SIRT1 and −3, but SIRT4 is unchanged (178, 179), to allow for efficient mitochondrial activity and increased metabolism of glutamine. In summary, these data strongly support a model that SIRT4 functions as a negative regulator of mitochondrial metabolism, contrary and complementary to its mitochondrial relative SIRT3.…”

Section: Sirt4mentioning

confidence: 99%

Who watches the watchmen? Regulation of the expression and activity of sirtuins

2016

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Sirtuins (SIRT1-7) are a family of nicotine adenine dinucleotide (NAD)-dependent enzymes that catalyze post-translational modifications of proteins. Together, they regulate crucial cellular functions and are traditionally associated with aging and longevity. Dysregulation of sirtuins plays an important role in major diseases, including cancer and metabolic, cardiac, and neurodegerative diseases. They are extensively regulated in response to a wide range of stimuli, including nutritional and metabolic challenges, inflammatory signals or hypoxic and oxidative stress. Each sirtuin is regulated individually in a tissue- and cell-specific manner. The control of sirtuin expression involves all the major points of regulation, including transcriptional and post-translational mechanisms and microRNAs. Collectively, these mechanisms control the protein levels, localization, and enzymatic activity of sirtuins. In many cases, the regulators of sirtuin expression are also their substrates, which lead to formation of intricate regulatory networks and extensive feedback loops. In this review, we highlight the mechanisms mediating the physiologic and pathologic regulation of sirtuin expression and activity. We also discuss the consequences of this regulation on sirtuin function and cellular physiology.-Buler, M., Andersson, U., Hakkola, J. Who watches the watchmen? Regulation of the expression and activity of sirtuins.

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“…Blood samples were obtained from the cut tip of the tail at 0, 30, 60, 90 and 120 min after glucose administration for glucose determination using a glucose analyser (Accu‐Chek Advantage; Roche Diagnostics, Rotkreuz, Switzerland) (do Amaral et al . ).…”

Section: Methodsmentioning

confidence: 97%

“…We previously demonstrated that a 40% reduction in food restriction decreases insulin secretion stimulated by glucose and depolarizing agents, an effect associated with lower glucose oxidation and a reduction in the expression of the silent information regulator‐T1 (SIRT1) protein (do Amaral et al . ). However, increased SIRT1 was associated with the effects of chronic calorie restriction, and a relationship between SIRT1 and AMP‐activated kinase (AMPK) was reported (Chen et al .…”

mentioning

confidence: 97%

“…Caloric restriction (CR) modulates molecular and biochemical pathways that delay physiopathological alterations associated with ageing and prevent diseases such as hypertension, obesity and diabetes (Cant o & Auwerx 2009). We previously demonstrated that a 40% reduction in food restriction decreases insulin secretion stimulated by glucose and depolarizing agents, an effect associated with lower glucose oxidation and a reduction in the expression of the silent information regulator-T1 (SIRT1) protein (do Amaral et al 2011). However, increased SIRT1 was associated with the effects of chronic calorie restriction, and a relationship between SIRT1 and AMP-activated kinase (AMPK) was reported (Chen et al 2010;Wang et al 2012;Chen et al 2013).…”

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confidence: 99%

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Reduced AMPKα2 protein expression restores glucose‐induced insulin secretion in islets from calorie‐restricted rats

Amaral

Ribeiro

Vanzela

et al. 2016

Int J Experimental Path

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SUMMARYIn a state of caloric restriction (CR), improved insulin action was associated with the activation of AMP-activated kinase (AMPK). Here, we verified whether AMPK was involved in impaired b-cell function in islets from rats subjected to CR for 21 days. Eight-week-old male rats were distributed into a control (CTL) group that was fed an isocaloric diet ad libitum or a CR group that received 60% of the food consumed by the CTL group. From days 18-21, CTL and CR rats were treated with sense (CTLS and CRS) or antisense (CTLAS and CRAS) AMPKa2 oligonucleotides. Caloric restriction was associated with decreased body weight, perigonadal fat pads and insulinaemia, while higher glucose tolerance was observed in CRS rats. Antisense treatment normalized insulinaemia and glucose tolerance in CRAS rats and increased cholesterolaemia in CRAS and CTLAS groups. These effects were associated with reduced pAMPK/AMPK protein expression in the liver of rats treated with antisense oligonucleotides. Additionally, CRS islets showed higher pAMPK/ AMPK content and lower glucose-induced insulin release. As expected, antisense oligonucleotides against AMPKa2 efficiently reduced pAMPK/AMPK protein in CRAS and CTLAS islets. The lower AMPK content in CRAS islets normalized the insulin secretion in islets exposed to 16.7 mM glucose. In addition, CTLAS islets presented higher insulin secretion at 2.8 and 16.7 mM glucose. These findings support the hypothesis that higher AMPK protein expression is involved in impaired b-cell function in islets from rats subjected to CR for 21 days.

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Reduced expression of SIRT1 is associated with diminished glucose-induced insulin secretion in islets from calorie-restricted rats

Cited by 22 publications

References 35 publications

Metabolic programming effects initiated in the suckling period predisposing for adult-onset obesity cannot be reversed by calorie restriction

Metabolic programming effects initiated in the suckling period predisposing for adult-onset obesity cannot be reversed by calorie restriction

Who watches the watchmen? Regulation of the expression and activity of sirtuins

Reduced AMPKα2 protein expression restores glucose‐induced insulin secretion in islets from calorie‐restricted rats

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