Sleep disturbance and appetite loss after lovastatin

Sinzinger, H.; Mayr, Friedrich; Schmid, Peter; Granegger, Susanne; O’Grady, John; Peskar, B.

doi:10.1016/s0140-6736(94)90094-9

Cited by 26 publications

(10 citation statements)

References 6 publications

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“…Furthermore, consistent with our finding, the previous studies revealed that statins reduced body weight gain in experimental animals [20]. Another investigation reported that statins might induce body weight loss via decreased appetite [21]. Based on these findings, we may infer that rosuvastatin reduced body weight gain in cirrhotic rats via decreased oral intake.…”

Section: Discussionsupporting

confidence: 91%

Rosuvastatin improves hepatopulmonary syndrome through inhibition of inflammatory angiogenesis of lung

et al. 2015

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The hepatopulmonary syndrome (HPS) is characterized by hypoxia and increased intrapulmonary shunts in cirrhotic patients. Emerging evidence showed promising results of treating HPS by abolishment of intrapulmonary inflammation and angiogenesis. Rosuvastatin is a kind of 3-hydroxy-methyl-3-glutamyl coenzyme A reductase inhibitor. In addition to lipid-lowering effects, it has anti-inflammation and anti-angiogenesis properties. We postulated that rosuvastatin treatment can ameliorate HPS. Common bile duct ligation (CBDL) was applied in an experimental HPS animal model. CBDL rats received 2-week rosuvastatin (20 mg/kg/day) treatments from the fifteenth day after operation. The haemodynamic data, blood gas analysis, liver biochemistries, tumour necrosis factor-α (TNF-α) and vascular endothelial growth factor (VEGF) were examined after rosuvastatin treatment. The liver and lung tissues were dissected for histopathological studies and protein analyses. In the parallel groups, intrapulmonary shunts were determined. The haemodynamic and liver biochemistries were not changed after rosuvastatin treatment in CBDL rats, but the alveolar-arterial oxygen pressure gradient was significantly decreased, implying that HPS-induced hypoxia was reversed after rosuvastatin treatment. In addition, rosuvastatin treatment reduced intrapulmonary shunts and plasma levels of VEGF and TNF-α. Besides, the intrapulmonary protein expression of nuclear factor kappa B (NF-κB), VEGF receptor (VEGFR)-1,2 and Rho-associated A kinase were significantly down-regulated and the intrapulmonary angiogenesis was ameliorated. We concluded that rosuvastatin alleviates experimental HPS through blockade of pulmonary inflammatory angiogenesis via TNF-α/NF-κB and VEGF/Rho-associated A kinase pathways down-regulation.

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Section: Discussionsupporting

confidence: 91%

Rosuvastatin improves hepatopulmonary syndrome through inhibition of inflammatory angiogenesis of lung

et al. 2015

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“…Consumption of the HF diet resulted in a decrease in food consumption; however, energy intake in the HF group was 22.4% (Po0.001) higher than that in the control group. In accordance with a previous study 37 in which lovastatin reduced the food/energy consumption by Prevention of obesity by red mold rice W-P Chen et al 10.7% (Po0.05), lovastatin reduced the food/energy consumption by 12.9% (Po0.01) in this study, but only in the high-dose RMR group (2%, w w…”

supporting

confidence: 93%

“…It appears that the inhibitory effect of RMR on appetite is related to the monacolin K component. 37 As expected, RMR supplementation normalized the dyslipidemia induced by the HF diet. Lovastatin is a competitive inhibitor of HMG-CoA reductase, the major rate-limiting enzyme in the cholesterol biosynthesis pathway, which has been introduced to the clinic for the treatment of hypercholesterolemia.…”

supporting

confidence: 71%

Red mold rice prevents the development of obesity, dyslipidemia and hyperinsulinemia induced by high-fat diet

Chen

Lee

et al. 2008

Int J Obes

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Objective: To investigate the influences of red mold rice (RMR) on obesity and related metabolic abnormalities. Methods and results:The 3T3-L1 cell line was used to examine the effects of RMR extracts on preadipocytes and on mature adipocytes. Both water and ethanol extracts of RMR had inhibitory effects on 3T3-L1 preadipocyte proliferation and differentiation. Water extracts of RMR enhanced the lipolysis activity in mature adipocytes, which negatively correlated with the triglyceride content within cells. RMR treatment did not affect heparin-releasable lipoprotein lipase activity in mature adipocytes. Furthermore, animal studies were carried out to explore the antiobesity effects of RMR. The control group of male Wistar rats were fed regular laboratory feed, whereas the other groups were fed the high-fat (HF) diet supplemented with lovastatin, rice or RMR (0.4 and 2%, w w À1 ). The relative caloric intakes of the control and HF groups were 3.34 and 4.85 kcal g À1 , respectively. After 6 weeks, rats treated with RMR at the 0.4 and 2% doses had lower weight gain and less fat pads mass accompanied with smaller fat cells than did the HF-diet rats. These effects probably resulted from an increase in the lipolysis activity of adipose tissue and a reduction in food/energy consumption. On the other hand, the RMR supplement significantly reduced serum total cholesterol, serum low-density lipoprotein (LDL) cholesterol, the ratio of LDL to high-density lipoprotein (HDL) cholesterol and serum insulin in the HF group. Moreover, the 2% RMR treatment significantly increased serum HDL cholesterol. Conclusion: This study reveals for the first time that RMR can prevent body fat accumulation and improve dyslipidemia. The antiobesity effects of RMR mainly derive from the lipolytic activity and mild antiappetite potency of RMR. In addition, extracts of RMR suppressed the proliferation and differentiation in 3T3-L1 preadipocytes, which might have contributed to the inhibition of new adipocyte formation or hyperplasia in adipose tissue.

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“…However, results might differ in individuals with history of or risk factors for hemorrhagic stroke Blood glucose -High-dose statins led to a statistically significant increase in glycemia in the -This supplements data seen in another PROVE-IT-TIMI trial [185] RCT, showing significant but small average -In the JUPITER trial, those randomized to rosuvastatin 20 mg versus placebo increase in HbA1c with (non-high-dose) showed a significant increase in HbA1c (p = 0.001) and in newly diagnosed statins [184] diabetes mellitus (relative risk 1.25; p = 0.01) [191] -Lower dose statins have not led to average increases in glycemia in most trials, but case reports clarify that large increases can arise in selected individuals reproducibly with statins [183,527] -One observational study reports that patients on statins may be less likely to develop diabetes mellitus after renal transplant; [528] however (particularly in light of the PROVE-IT-TIMI results), this could reflect indication bias Sleep Significant reductions in average sleep quality were seen with simvastatin but not -Also, case reports and case series of pravastatin relative to placebo. [447] However, 'much worse' sleep (relative to sleep problems [444,[529][530][531][532][533] and 'much better') was significantly more common with each of the two statins nightmares; [534,535] and reports of sleep AEs relative to placebo, suggesting that statin sleep AEs may be seen with both in clinical trials of statins [536][537][538] agents [447] -A small study reported development of objective sleep problems on lovastatin but not pravastatin [539] (although other small studies reported no objective findings) -In one statin AE evaluation study in Spain, 26 statin patients were referred for oral evaluation; however, it was noted that 17% of these subjects cited insomnia, with 16/17 improving with interruption of statin treatment [540] a For the sample employed in that RCT. Effect modification can lead to effects that differ in different samples.…”

Section: Phillipsmentioning

confidence: 99%

Statin Adverse Effects

Golomb

Evans

2008

American Journal of Cardiovascular Drugs

592

257

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HMG-CoA reductase inhibitors (statins) are a widely used class of drug, and like all medications, have potential for adverse effects (AEs). Here we review the statin AE literature, first focusing on muscle AEs as the most reported problem both in the literature and by patients. Evidence regarding the statin muscle AE mechanism, dose effect, drug interactions, and genetic predisposition is examined. We hypothesize, and provide evidence, that the demonstrated mitochondrial mechanisms for muscle AEs have implications to other nonmuscle AEs in patients treated with statins. In meta-analyses of randomized controlled trials (RCTs), muscle AEs are more frequent with statins than with placebo. A number of manifestations of muscle AEs have been reported, with rhabdomyolysis the most feared. AEs are dose dependent, and risk is amplified by drug interactions that functionally increase statin potency, often through inhibition of the cytochrome P450 3A4 system. An array of additional risk factors for statin AEs are those that amplify (or reflect) mitochondrial or metabolic vulnerability, such as metabolic syndrome factors, thyroid disease, and genetic mutations linked to mitochondrial dysfunction. Converging evidence supports a mitochondrial foundation for muscle AEs associated with statins, and both theoretical and empirical considerations suggest that mitochondrial dysfunction may also underlie many nonmuscle statin AEs. Evidence from RCTs and studies of other designs indicates existence of additional statin-associated AEs, such as cognitive loss, neuropathy, pancreatic and hepatic dysfunction, and sexual dysfunction. Physician awareness of statin AEs is reportedly low even for the AEs most widely reported by patients. Awareness and vigilance for AEs should be maintained to enable informed treatment decisions, treatment modification if appropriate, improved quality of patient care, and reduced patient morbidity.

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Sleep disturbance and appetite loss after lovastatin

Cited by 26 publications

References 6 publications

Rosuvastatin improves hepatopulmonary syndrome through inhibition of inflammatory angiogenesis of lung

Rosuvastatin improves hepatopulmonary syndrome through inhibition of inflammatory angiogenesis of lung

Red mold rice prevents the development of obesity, dyslipidemia and hyperinsulinemia induced by high-fat diet

Statin Adverse Effects

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