scholarly journals Effects of low‐dose metformin on pre‐frailty among middle‐aged and elderly pre‐diabetic people

2022 ◽  
Author(s):  
Chun‐Feng Huang ◽  
Ming‐Shi Shiao ◽  
Tso‐Yen Mao
Keyword(s):  
Low Dose ◽  
1990 ◽  
Vol 84 (2-3) ◽  
pp. 203-211 ◽  
Author(s):  
Cesare R. Sirtori ◽  
Laura Calabresi ◽  
Guido Franceschini ◽  
Gemma Gianfranceschi ◽  
Francesco Zoppi ◽  
...  

2009 ◽  
Vol 106 (2) ◽  
pp. 500-505 ◽  
Author(s):  
Lacy A. Holowatz ◽  
W. Larry Kenney

Full expression of reflex cutaneous vasodilation is dependent on cyclooxygenase- (COX) and nitric oxide synthase- (NOS) dependent mechanisms. Low-dose aspirin therapy is widely prescribed to inhibit COX-1 in platelets for atherothrombotic prevention. We hypothesized that chronic COX inhibition with daily low-dose aspirin therapy (81 mg) would attenuate reflex vasodilation in healthy human skin. Two microdialysis fibers were placed in forearm skin of seven middle-aged (57 ± 3 yr), normotensive, healthy humans with no preexisting cardiovascular disease, taking daily low-dose aspirin therapy (aspirin: 81 mg), and seven unmedicated, healthy, age-matched control (no aspirin, 55 ± 3 yr) subjects, with one site serving as a control (Ringer) and the other NOS inhibited (NOS inhibited: 10 mM NG-nitro-l-arginine methyl ester). Red cell flux was measured over each site by laser-Doppler flowmetry, as reflex vasodilation was induced by increasing core temperature (oral temperature) 1.0°C using a water-perfused suit. Cutaneous vascular conductance (CVC) was calculated (CVC = flux/mean arterial pressure) and normalized to maximal CVC (CVCmax; 28 mM sodium nitroprusside). CVCmax was not affected by either aspirin or NOS inhibition. The plateau in cutaneous vasodilation during heating (change in oral temperature = 1.0°C) was significantly attenuated in the aspirin group (aspirin: 25 ± 3% CVCmax vs. no aspirin: 50 ± 7% CVCmax, P < 0.001 between groups). NOS inhibition significantly attenuated %CVCmax in both groups (aspirin: 17 ± 2% CVCmax, no aspirin: 23 ± 3% CVCmax; P < 0.001 vs. control), but this attenuation was less in the no-aspirin treatment group ( P < 0.001). This is the first observation that chronic low-dose aspirin therapy attenuates reflex cutaneous vasodilation through both COX- and NOS-dependent mechanisms.


2010 ◽  
Vol 108 (6) ◽  
pp. 1575-1581 ◽  
Author(s):  
Lacy A. Holowatz ◽  
John D. Jennings ◽  
James A. Lang ◽  
W. Larry Kenney

Chronic systemic platelet cyclooxygenase (COX) inhibition with low-dose aspirin [acetylsalicylic acid (ASA)] significantly attenuates reflex cutaneous vasodilation in middle-aged humans, whereas acute, localized, nonisoform-specific inhibition of vascular COX with intradermal administration of ketorolac does not alter skin blood flow during hyperthermia. Taken together, these data suggest that platelets may be involved in reflex cutaneous vasodilation, and this response is inhibited with systemic pharmacological platelet inhibition. We hypothesized that, similar to ASA, specific platelet ADP receptor inhibition with clopidogrel would attenuate reflex vasodilation in middle-aged skin. In a double-blind crossover design, 10 subjects (53 ± 2 yr) were instrumented with four microdialysis fibers for localized drug administration and heated to increase body core temperature [oral temperature (Tor)] 1°C during no systemic drug (ND), and after 7 days of systemic ASA (81 mg) and clopidogrel (75 mg) treatment. Skin blood flow (SkBF) was measured using laser-Doppler flowmetry over each site assigned as 1) control, 2) nitric oxide synthase inhibited (NOS-I; 10 mM NG-nitro-l-arginine methyl ester), 3) COX inhibited (COX-I; 10 mM ketorolac), and 4) NOS-I + COX-I. Data were normalized and presented as a percentage of maximal cutaneous vascular conductance (%CVCmax; 28 mM sodium nitroprusside + local heating to 43°C). During ND conditions, SkBF with change (Δ) in Tor = 1.0°C was 56 ± 3% CVCmax. Systemic low-dose ASA and clopidogrel both attenuated reflex vasodilation (ASA: 43 ± 3; clopidogrel: 32 ± 3% CVCmax; both P < 0.001). In all trials, localized COX-I did not alter SkBF during significant hyperthermia (ND: 56 ± 7; ASA: 43 ± 5; clopidogrel: 35 ± 5% CVCmax; all P > 0.05). NOS-I attenuated vasodilation in ND and ASA (ND: 28 ± 6; ASA: 25 ± 4% CVCmax; both P < 0.001), but not with clopidogrel (27 ± 4% CVCmax; P > 0.05). NOS-I + COX-I was not different compared with NOS-I alone in either systemic treatment condition. Both systemic ASA and clopidogrel reduced the time required to increase Tor 1°C (ND: 58 ± 3 vs. ASA: 45 ± 2; clopidogrel: 39 ± 2 min; both P < 0.001). ASA-induced COX and specific platelet ADP receptor inhibition attenuate reflex vasodilation, suggesting platelet involvement in reflex vasodilation through the release of vasodilating factors.


Author(s):  
Qike Jia ◽  
Hongliang Chen ◽  
Xuewei Chen ◽  
Qichuan Tang

Purpose: The current study aims to explore the barriers for middle-aged Chinese to learn about and uptake low-dose computed tomography (LDCT) lung cancer screening. Methods: Data were collected via an online survey in December 2019. Final valid sample included 640 respondents, aged 40–60 years old, from 21 provinces of China. We performed multiple linear regressions to test the potential barriers to LDCT scan. Findings: Cost concerns, distrust in doctors, fears of disease, lack of knowledge, and optimistic bias are negatively associated with the intention to learn about and uptake LDCT scan. Implications: Our study contributes to understanding the negative predictors of middle-aged Chinese to get LDCT lung cancer scans. Future campaign programs should help audiences to build comprehensive understandings about lung cancer and LDCT scan. To better promote LDCT scan in China, the government should fund more trial programs continuously and public efforts should be made to rebuild the patient–doctor trust.


2019 ◽  
Vol 20 (8) ◽  
pp. 1844 ◽  
Author(s):  
Miodrag Janić ◽  
Mojca Lunder ◽  
Srdjan Novaković ◽  
Petra Škerl ◽  
Mišo Šabovič

The incidence of aging-related disorders may be decreased through strategies influencing the expression of longevity genes. Although numerous approaches have been suggested, no effective, safe, and easily applicable approach is yet available. Efficacy of low-dose fluvastatin and valsartan, separately or in combination, on the expression of the longevity genes in middle-aged males, was assessed. Stored blood samples from 130 apparently healthy middle-aged males treated with fluvastatin (10 mg daily), valsartan (20 mg daily), fluvastatin-valsartan combination (10 and 20 mg, respectively), and placebo (control) were analyzed. They were taken before and after 30 days of treatment and, additionally, five months after treatment discontinuation. The expression of the following longevity genes was assessed: SIRT1, PRKAA, KLOTHO, NFE2L2, mTOR, and NF-κB. Treatment with fluvastatin and valsartan in combination significantly increased the expression of SIRT1 (1.8-fold; p < 0.0001), PRKAA (1.5-fold; p = 0.262) and KLOTHO (1.7-fold; p < 0.0001), but not NFE2L2, mTOR and NF-κB. Both fluvastatin and valsartan alone significantly, but to a lesser extent, increased the expression of SIRT1, and did not influence the expression of other genes. Five months after treatment discontinuation, genes expression decreased to the basal levels. In addition, analysis with previously obtained results revealed significant correlation between SIRT1 and both increased telomerase activity and improved arterial wall characteristics. We showed that low-dose fluvastatin and valsartan, separately and in combination, substantially increase expression of SIRT1, PRKAA, and KLOTHO genes, which may be attributed to their so far unreported pleiotropic beneficial effects. This approach could be used for prevention of ageing (and longevity genes)–related disorders.


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