Abstract Background Browning of white adipose tissue (WAT) is a promising approach to obesity treatment. During browning, WAT transforms into beige adipose tissue through stimulation of the peroxisome proliferator activated receptor γ (PPARγ). Nutmeg, one of the Indonesian herbs, reportedly has dual roles as a PPARα/γ partial agonist. Even though nutmeg has been traditionally used in body weight reduction, there is limited information regarding the potential role of nutmeg in browning of WAT. Objectives In this study, we explored the effect of nutmeg seed extract (NuSE) as a potential inductor of WAT browning. Methods Twelve male Wistar rats, 5–6 weeks old, were divided into control and nutmeg groups. The rats in nutmeg group were given NuSE for 12 weeks by oral gavage. After 12 weeks, the rat's inguinal WAT and brown adipose tissue (BAT) were collected, weighed and stored at − 80°C until use. Results We observed that even though NuSE did not reduce the final body weight, it significantly reduced body weight gain. NuSE also increased protein levels of peroxisome proliferator activated receptor γ coactivator 1α (PGC‐1α) and uncoupling protein 3 (UCP3) significantly and tended to increase UCP2 and UCP1 levels. Furthermore, NuSE induced macroscopic and microscopic morphological changes of inguinal WAT, marked by significantly increased adipocyte numbers and decreased adipocyte size. Conclusions Even though NuSE did not increase UCP1 significantly, it potentially alters inguinal WAT characteristics and leads to browning through PGC‐1α and UCP3 induction. However, UCP3’s specific mechanism in WAT browning remains unclear. Our findings could contribute to obesity treatment in the future.
The integration of combined aerobic exercise and intermittent fasting (IF) has emerged as a strategy for the prevention and management of obesity, including its associated health issues such as age-related metabolic diseases. This study aimed to examine the potential of combined aerobic exercise and IF as a preventative strategy against cellular senescence by targeting mTOR and Bcl-2 levels in obese females. A total of 30 obese women, aged 23.56 ± 1.83 years, body fat percentage (FAT) 45.21 ± 3.73% (very high category), BMI 30.09 ± 3.74 kg/m2 were recruited and participated in three different types of interventions: intermittent fasting (IF), exercise (EXG), and a combination of intermittent fasting and exercise (IFEXG). The intervention program was carried out 5x/week for 2 weeks. We examined mTOR and Bcl-2 levels using ELISA kits. Statistical analysis used the one-way ANOVA test and continued with Tukey’s HSD post hoc test, with a significance level of 5%. The study results showed that a combination of aerobic exercise and IF significantly decreased mTOR levels (−1.26 ± 0.79 ng/mL) compared to the control group (−0.08 ± 1.33 ng/mL; p ≤ 0.05). However, combined aerobic exercise and IF did not affect Bcl-2 levels significantly (−0.07 ± 0.09 ng/mL) compared to the control group (0.01 ± 0.17 ng/mL, p ≥ 0.05). The IF-only group, exercise-only group, and combined group all showed a significant decrease in body weight and fat mass compared to the control group (p ≤ 0.05). However, the combined aerobic exercise and IF program had a significant effect in reducing the total percentage of body fat and fat mass compared to the IF-only group (p ≤ 0.05). Therefore, it was concluded that the combined intermittent fasting and exercise group (IFEXG) undertook the most effective intervention of the three in terms of preventing cellular senescence, as demonstrated by decreases in the mTOR level, body weight, and fat mass. However, the IFEXG did not present reduced Bcl-2 levels.
ABSTRAK Sindroma metabolik (SM) merupakan masalah kesehatan yang meningkat di seluruh dunia. Di Indonesia, angka penderita sindroma metabolik mencapai 21,8%. Penderita SM meningkat pada lansia karena telah terjadi berbagai kelainan metabolisme. Sehingga diperlukan peningkatan kesadaran masyarakat mengenai komplikasi SM. Masyarakat juga diharapkan untuk mengendalikan faktor resiko SM seperti pengaturan pola aktivitas fisik. Aktifitas fisik seperti olahraga telah terbukti dapat menurunkan resistensi insulin dan memperbaiki profil lipid. Penyuluhan mengenai komplikasi SM dan pengendaliannya dengan cara meningkatkan aktivitas fisik diharapkan dapat memberikan edukasi pada masyarakat. Kegiatan yang dilakukan berupa wawancara mengenai pengetahuan masyarakat mengenai SM dan olahraga yang tepat dalam penanganan sindroma metabolik. Survey pada masyarakat menunjukkan sebagian besar masyarakat (72%) telah mengetahui sindroma metabolik, namun tidak mengetahui penyakit yang dapat disebabkan oleh SM (63%). Disamping itu, hanya 55% responden yang megetahui pengaruh olahraga dalam perbaikan SM. Kegiatan dilanjutkan dengan penyuluhan dan tanya jawab mengenai SM. Melalui kegiatan pengabdian pada masyarakat ini, diharapkan terjadi perubahan gaya hidup di masyarakat sehingga SM dapat diatasi. Kata Kunci: Lansia, Olahraga, Penyuluhan, Sindroma Metabolik ABSTRACT Metabolic syndrome (MS) prevalence is increasing worldwide. In Indonesia, MS prevalence was 21.8% in 2018. MS is a risk factor for cardiovascular disease and diabetes. MS risk factor is increased in the elderly. An increase in physical activity has been proven to reduce the MS risk factor. Thus, behavioral changes are the key factor to manage MS. In this community service, we gave education to the elderly population in the Cimahi area, Bandung, West Java about MS was done prior to the education. We found that most of the community members already know about MS. However, only 55% of respondents understand a complication of MS. To educate the local people about the MS prevention program, we gave seminars and counseling. Changes in behavior including diet programs and exercise are the key factor to prevent MS. Keywords: Elderly, Education, Metabolic Syndrome, Physical Exercise
Pemberian asam traneksamat (AT) per oral telah terbukti dapat mengurangi keriput yang diinduksi oleh kulit kering pada mencit. Namun, dosis oral yang setara terlalu besar untuk digunakan pada manusia dalam jangka panjang karena dapat menimbulkan toksisitas, sehingga perlu dicari sediaan alternatif lain secara topikal seperti sediaan krim. Penelitian ini bertujuan untuk menganalisis pengaruh pemberian krim AT terhadap pembentukan keriput pada kulit mencit jantan galur Balb/c yang dipajan sinar ultraviolet B (UVB). Penelitian dilakukan terhadap 24 ekor mencit di Laboratorium Farmakologi dan Terapi serta Laboratorium Sentral Universitas Padjadjaran pada bulan Februari hingga Mei 2018. Mencit dibagi secara acak ke dalam empat kelompok, yaitu satu kelompok kontrol (P0) hanya mendapatkan pajanan sinar UVB tanpa krim AT dan tiga kelompok perlakuan (P1, P2, dan P3) mendapat pajanan sinar UVB dan diberikan krim AT dengan konsentrasi masing-masing 3%, 4%, dan 5%. Setelah 10 minggu, dilakukan penilaian kondisi keriput pada kulit punggung mencit berdasarkan metode Bisett , dilanjutkan dengan biopsi kulit punggung mencit untuk pemeriksaan kadar matriks metaloproteinase-1 (MMP-1) dengan teknik western blot (WB). Diperoleh perbedaan nilai rata-rata skor keriput yang bermakna sebesar 2,1±0,105 pada kelompok P0, 1,1±0,167 pada P1 dan P2, serta 1,3±0,211 pada P3 (p=0,005). Diperoleh pula nilai rata-rata kadar MMP-1 yang bermakna, yakni sebesar 0,75±0,08 pada kelompok P0, serta 0,54±0,033, 0,40±0,052, dan 0,54±0,072 pada P1, P2, dan P3 secara berturut-turut (p=0,008). Berdasarkan hasil tersebut, dapat disimpulkan bahwa pemberian krim AT mampu memperlambat pembentukan keriput dan menurunkan kadar MMP-1 pada kulit punggung mencit jantan galur Balb/c yang dipajan sinar UVB. Kata kunci: Keriput, krim asam traneksamat, matriks metaloproteinase-1, sinar ultraviolet B The Effect of Tranexamic Acid Cream on Wrinkle Formation and Matrix Metalloproteinase-1 Levels on Male Balb/c Mice Skin Exposed to Ultraviolet B Radiations Abstract Oral tranexamic acid (TXA) has been proven to ameliorate wrinkle induced by skin dryness in hairless mouse. However, the equal human oral dose is too high and can induce toxicity if used in long term, and study of topical preparations for wrinkle treatment is limited. Therefore, this study was conducted using topical preparations as an alternative for oral treatment to examine the effects of TXA cream in wrinkle formation. Four weeks old of twenty-four male Balb/c mice, divided into four groups, then 3%, 4% and 5% TXA cream were administered on the back skin of mice in each group shortly after ultraviolet B (UVB) exposure, except for control group that only exposed to UVB lights without given any TXA creams. Wrinkle formation and matrix metalloproteinase (MMP-1) level were observed after 10 weeks of treatments. There were significant differences of wrinkle score, with mean value were 2.1±0.105 for control group, 1.1±0.167 for 3% and 4% groups, and 1.3±0.211 for 5% group (p=0.005). There were also significant differences of MMP-1, with mean value were 0.75±0.08 for control group, 0.54±0.033, 0.40±0.052, and 0.54±0.072 for 3%, 4% and 5% group, respectively (p=0.008). Based on significant differences of wrinkle score and MMP-1 level, it can be concluded that administration of TXA cream may able to delay wrinkle formation and reduce the MMP-1 level on the mice skin exposed to ultraviolet B. Keywords: Matrix metalloproteinase-1, tranexamic acid, ultraviolet B, wrinkle
Sedentary lifestyle can cause the accumulation of energy reserves in the form of lipids in white adipose cells. Lifestyle modification by means of exercise is done to reduce fat reserves in white adipose tissue (WAT). This study aims to determine the effect of exercise in various intensities on the histological changes of white adipose cells. Research method exploratory with Federer formula to determine the number of samples carried out. Using 28 Wistar rats located at the Central Laboratory of Padjadjran University, Sumedang from May to June 2022. The data taken were the average diameter ± standard error (SEM) of the inguinal white adipose cells of the experimental rats. Data analysis using Microsoft Excel 2016 and SPSS v.28 software. Of the 28 samples studied, only 25 samples met the inclusion criteria. Group K is 0.15% (p = 0.024) greater than P2, and 0.25% (p 0.001) is greater than P3. The P1 group had a value of 0.17% (p = 0.025) greater than P3. Moderate and vigorous exercise can be used to reduce the size of white adipose cells. While low-intensity exercise is considered ineffective. Further research can be carried out to assess changes in white adipose cells based on exercise intensity from other sides besides their morphology.
Keywords: Histological, White Adipose Tissue, Exercise
The popularity of the electronic cigarette has soared in the last decades. However, the health effect of smoking electronic cigarettes on the vascular system is unclear. This systematic review examines the electronic cigarettes’ effect on the vascular system from recent evidence. A systematic search was conducted in MEDLINE (PubMed) database from January 2016 to August 2021 for studies assessing the vascular effect of chronic use of electronic cigarettes on human and animal. The Cochrane Risk of Bias 2, NIH Quality Assessment for Cross-Sectional Study, and SYRCLE’s Risk of Bias were used to assess the risk of bias in interventional, observational, and animal study, respectively. A narrative synthesis of evidence is provided to describe results. From 101 retrieved studies related to electronic cigarettes effect on the vascular system, a total of 16 studies are included in this review. The overall results indicated that electronic cigarette use is associated with adverse events in the vascular, including the incident of elevated oxidative stress, endothelial dysfunction, inflammation, arterial stiffness, and the development of atherosclerotic lesion. Further studies should broaden perspectives and reveal more about the mechanism of how electronic cigarettes impact on vascular system.
This study was conducted to evaluate the effect of Calcitriol on cellular death in HeLa cells via autophagy and turn over due to mitochondria homeostasis.HeLa cell lines were grown in 24-well plates and treated with Calcitriol at varying doses (0.013 μM-0.325 μM) for varying time periods (2, 6, 12, and 18 h). Cell proteins were extracted with scrapers and lysed using RIPA buffer. Western blots were performed for proteins involved with autophagy (Lc3, p62), signaling (mTOR, PI3K, HIF1α), mitochondria (PGC1α, COX4, and Tom 20), and apoptosis (Caspase 3, Caspase 9, and PARP). Protein carbonyl levels were determined by measuring the indirect ROS level. An inhibition study using L-mimosine was performed to analyze the significance of HIF1α.Calcitriol treatment induced cytotoxicity in a dose- and time-dependent manner and caused growth arrest in HeLa cells. The PI3K-AKT-mTOR pathway was activated, leading to inhibition of autophagy and alterations in mitochondria biogenesis homeostasis. Treatment with Calcitriol produced protein carbonyl levels similar to those in the cisplatin-treated and control groups. Increased ROS levels may cause toxicity and induce cell death specifically in cancer cells but not in normal cells. The inhibition of HIF1α partially rescued the HeLa cells from the toxic effects of Calcitriol treatment.We suggest that Calcitriol may shut down mitochondrial homeostasis in HeLa cells by inducing the PI3K-AKT-mTOR pathway and inhibiting autophagy, which leads to cell death.
Thyroid hormone (TH) and autophagy share similar functions in regulating skeletal muscle growth, regeneration, and differentiation. Although TH recently has been shown to increase autophagy in liver, the regulation and role of autophagy by this hormone in skeletal muscle is not known. Here, using both in vitro and in vivo models, we demonstrated that TH induces autophagy in a dose- and time-dependent manner in skeletal muscle. TH induction of autophagy involved reactive oxygen species (ROS) stimulation of 5'adenosine monophosphate-activated protein kinase (AMPK)-Mammalian target of rapamycin (mTOR)-Unc-51-like kinase 1 (Ulk1) signaling. TH also increased mRNA and protein expression of key autophagy genes, microtubule-associated protein light chain 3 (LC3), Sequestosome 1 (p62), and Ulk1, as well as genes that modulated autophagy and Forkhead box O (FOXO) 1/3a. TH increased mitochondrial protein synthesis and number as well as basal mitochondrial O2 consumption, ATP turnover, and maximal respiratory capacity. Surprisingly, mitochondrial activity and biogenesis were blunted when autophagy was blocked in muscle cells by Autophagy-related gene (Atg)5 short hairpin RNA (shRNA). Induction of ROS and 5'adenosine monophosphate-activated protein kinase (AMPK) by TH played a significant role in the up-regulation of Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PPARGC1A), the key regulator of mitochondrial synthesis. In summary, our findings showed that TH-mediated autophagy was essential for stimulation of mitochondrial biogenesis and activity in skeletal muscle. Moreover, autophagy and mitochondrial biogenesis were coupled in skeletal muscle via TH induction of mitochondrial activity and ROS generation.
