Jean Sparks

Kalanchoe pinnata, commonly known as the “miracle plant” or “life plant”, is a succulent species traditionally used for various health conditions. Recent research investigations have intensified interest in this species due to its diverse repertoire of bioactive constituents, including flavonoids, alkaloids, triterpenes, and glycosides. These compounds have been associated with multiple therapeutic effects, notably antioxidant, anti-inflammatory, and antidiabetic activities. Although several studies have highlighted the positive effects of the extracts of K. pinnata on key factors contributing to the pathophysiology and complications of diabetes mellitus, a systematic overview focusing on the use of these extracts and their bioactive constituents in the management of the disease is lacking. This literature review summarizes the phytochemical composition, traditional uses, and recent scientific data supporting the antidiabetic potential of K. pinnata, with a particular focus on its effects on glycemic control, as well as inflammatory and oxidative homeostasis, toxicity, safety, and potential clinical implications. The phytochemical constituents discussed include quercetin, kaempferol, apigenin, epigallocatechin gallate (EGCG), avicularin, and bufadienolides, along with a presentation of representative structures. The review also covers the potential mechanisms of action in diabetes mellitus. The survey of available literature highlights the effects of K. pinnata on indices of diabetes mellitus, including enhancing insulin sensitivity, mitigating oxidative stress and inflammation, lowering blood glucose levels, and the potential adverse effects. These results point to the promising prospect for K. pinnata use in the management of diabetes mellitus and its associated complications, while underscoring the need for more rigorous investigations, including well-controlled clinical trials.

Background: Intermittent fasting has become a new fad diet that may promote an environment to facilitate muscle atrophy, placing aging, and diabetic populations at risk for muscle loss due to nutrient deprivation. The purpose of this study was to investigate how nutrient availability and serum environment influence Type 2 diabetic myoblast density and viability, autophagy‐related oxidative and inflammatory markers, and upstream gene expression signaling relevant to proteostasis. Methods: To explore this outcome in human skeletal muscle myoblast (HSMM) and diabetic human skeletal muscle myoblast (D‐HSMM), myoblast lines were cultured per standard protocol and were incubated for 12 or 24 h with either human serum (HS) or fetal bovine serum (FBS) at varying serum media concentrations: 5%, 10%, and 15%. Cell viability and density were determined; ELISAs were used to assess SOD1 and TNFα; TaqMan gene array plates were used to explore mRNA gene expression related to growth and atrophy. Results: Cell viability (%) analysis showed that 0% concentration, 12 h incubation, and FBS media have lower viability ( p ≤ 0.0001); cell density analysis showed lower values in 0% concentration and in the FBS media ( p ≤ 0.0001); SOD1 analysis showed a scaled effect ( p ≤ 0.05) and higher concentration in HS (12,795.07 ± 677.87 pg/mL; p ≤ 0.0001); TNFα concentration was higher in HSMM compared to D‐HSMM (61 ± 0.82 vs. 2.52 ± 0.94 pg/mL; p = 0.017), higher at 12 h (6.07 ± 0.88 vs. 2.50 ± 0.88 pg/mL; p = 0.006), and higher in FBS (6.05 ± 0.88 vs. 2.08 ± 0.88 pg/mL; p = 0.002); no meaningful increase in fold change was seen in mRNA. Conclusions: Myoblast viability and density were lower in the nutrient‐deprived conditions and in the FBS compared to the HS serum. The biomarker of oxidative stress was lower in the serum concentration in a scaled effect, yet higher in HS. The biomarker of inflammation was higher in the HSMM cell line, shorter incubation time period, and in FBS. HS used as a media may supply nutrients and hormonal confounders that may support or stress myoblast growth.

With healthcare costs rising, many affected by ailments are turning to alternative medicine for treatment. More people are choosing to complement their pharmacological regimen with dietary supplements from natural products. In this study, the compound composition of Kalanchoe Pinnata (K. pinnata) and the effects of combined preparations of K. pinnata and metformin on antioxidant activity in human skeletal muscle myoblasts (HSMMs) and human diabetic skeletal muscle myoblasts (DHSMMs) were investigated. Ultraperformance liquid chromatography fusion orbitrap mass spectrometry (UPLC-OT-FTMS) identified biologically active flavanols in K. pinnata. The main compounds identified in locally grown K. pinnata were quercetin, kaempferol, apigenin, epigallocatechin gallate (EGCG), and avicularin. Antioxidant results indicated that a combinatorial preparation of K. pinnata with metformin may modulate antioxidant responses by increasing the enzymatic activity of superoxide dismutase and increasing levels of reduced glutathione. A combination of 50 μM and 150 μg/mL of metformin and K. pinnata, respectively, resulted in a significant increase in reduced glutathione levels in non-diabetic and diabetic human skeletal muscle myoblasts and H₂O_2-stress-induced human skeletal muscle myoblasts. Additionally, a K. pinnata treatment (400 µg/mL) alone significantly increased catalase (CAT) activity for non-diabetic and diabetic human skeletal muscle myoblasts and a H₂O_2-stress-induced human skeletal muscle myoblast cell line, while significantly lowering malondialdehyde (MDA) levels. However, the treatment options were more effective at promoting cell viability after 24 h versus 72 h and did not promote cell viability after 72 h in H₂O₂-stress-induced HSMM cells. These treatment options show promise for treating oxidative-stress-mediated pathophysiological complications associated with type II diabetes.

Background: Type 2 diabetes (T2D) is a chronic illness associated with resistance to or defective insulin secretion. This study investigates the effects of thermotherapy on cell viability, gene expression and inflammation in skeletal muscle cell lines. Methods: Healthy and T2D human skeletal muscle cell lines (HSMM and D-HSMM, respectively) were subjected to acute or chronic thermo-therapy (AT or CT, respectively). CT consisted of a 30 min exposure to 40 °C, three times a week for three weeks; AT was a one-time exposure. Results: A significant decrease in D-HSMM cell viability percentage followed AT; however, no significant change occurred in CT. HSMM yielded the highest elevations of genes following CT. In D-HSMM, both treatments yielded gene upregulation. Both treatments significantly down-regulated IL-1β, IL-6, IL-10 and TNF-α in HSMM. AT significantly decreased IL-1β, IL-6 and upregulated IL-10 and TNF-α levels in D-HSMM, while CT yielded a reduction in IL-4, TNF-α and an upregulation of IL-6 and IL-10. Conclusions: An increase in gene expression indicates actin activity and cellular responses, suggesting an increase in transcriptional regulation. The upregulation of IL-6 and IL-10 in D-HSMM negatively correlated with a decrease in TNF-α and IL-1β, indicating improved adverse inflammatory effects associated with the disease.

Diabetes mellitus is a chronic metabolic disease characterized by elevated blood glucose levels with associated disordered carbohydrate and lipid metabolism. Type 2 diabetes (T2D) specifically has been shown to cause a decrease in skeletal muscle mass due to oxidative stress. This study investigated a treatment option for T2D through thermotherapy on healthy (HSMM) and T2D (D-HSMM) human skeletal muscle cells. The goals were to determine the effects of thermotherapy, long-term (chronic) and short-term (acute), on HSMM and D-HSMM cell viabilities and oxidative stress. HSMM and D-HSMM cells were grown to confluency, harvested, and counted to determine density. Acute and chronic heat treatments were applied to both cell lines. The chronic treatment consisted of a 30-minute exposure to 40°C, three times a week for three weeks; the acute treatment was a one-time exposure. Oxidative stress assays and cell viabilities were tested 24 hours after heat treatments. Results indicated no significant effect on the cell viability of HSMM and D-HSMM cells. The acute treatment had a significant increase ( ) of MDA concentration compared to the chronic treatment. The chronic treatment had a significant increase ( ) in catalase activity compared to the acute treatment. The SOD activity had no significant change ( ) between the chronic and acute treatments. In conclusion, acute thermotherapy may not be beneficial for skeletal muscle cells due to the observed increase in oxidative stress, especially in the D-HSMM cells.