The role of 5′-adenosine monophosphate-activated protein kinase (AMPK) in skeletal muscle atrophy

As a key coordinator of metabolism, AMP-activated protein kinase (AMPK) is vitally involved in skeletal muscle maintenance. AMPK exerts its cellular effects through its function as a serine/threonine protein kinase by regulating many downstream targets and plays important roles in the development and growth of skeletal muscle. AMPK is activated by phosphorylation and exerts its function as a kinase in many processes, including synthesis and degradation of proteins, mitochondrial biogenesis, glucose uptake, and fatty acid and cholesterol metabolism. Skeletal muscle atrophy is a result of various diseases or disorders and is characterized by a decrease in muscle mass. The pathogenesis and therapeutic strategies of skeletal muscle atrophy are still under investigation. In this review, we discuss the role of AMPK in skeletal muscle metabolism and atrophy. We also discuss targeting AMPK for skeletal muscle treatment, including exercise, AMPK activators including 5-amino-4-imidazolecarboxamide ribonucleoside and metformin, and low-level lasers. These studies show the important roles of AMPK in regulating muscle metabolism and function; thus, the treatment of skeletal muscle atrophy needs to take into account the roles of AMPK.     

Molecular characterization of sweet potato (<i>Ipomoea batatas</i> [L.] Lam) germplasms for desirable traits by using simple sequence repeats markers

Every breeding program that aims to create new and improved cultivars with desired traits mostly relies oninformation related to genetic diversity. Therefore, molecular characterization of germplasms is important to obtain targetcultivars with desirable traits. Sweet potato [Ipomoea batatas (L.) Lam] is widely considered the world’s most important crop,with great diversity in morphological and phenotypic traits. The genetic diversity of 20 sweet potato germplasms originatingfrom Bangladesh, CIP, Philippines, Taiwan, and Malaysia were compared, which was accomplished by genetic diversityanalysis by exploring 20 microsatellite DNA markers for germplasm characterization and utilization. This information waseffective in differentiating or clustering the sweet potato genotypes. A total of 64 alleles were generated using the 20 primersthroughout the 20 germplasm samples, with locus IBS97 having the highest number of alleles (5), whereas locus IbU33 hadthe fewest alleles (2). The alleles varied in size from 105 (IbU31) to 213 base pairs (IBS34). The Polymorphism InformationContent (PIC) values for the loci IbL46 and IBS97 varied from 0.445 to 0.730. IBS97 has the highest number of effectivealleles (3.704), compared to an average of 2.520. The average Shannon’s diversity index (H) was 1.003, ranging from 0.673 inIbU3 to 1.432 in IBS97. The value of gene flow (Nm) varied between 0.000 and 0.005, with an average of 0.003, whereasgenetic differentiation (FST-values) ranged between 0.901 and 1.000. The sweet potato germplasm included in this study hada broad genetic base. SP1 vs. SP9 and SP12 vs. SP18 germplasm pairings had the greatest genetic distance (GD = 0.965),while SP1 vs. SP2 germplasm couples had the least genetic diversity (GD = 0.093). Twenty genotypes were classified into twogroups in the UPGMA dendrogram, with 16 genotypes classified as group “A” and the remaining four genotypes, SP10,SP18, SP19, and SP20, classified as group “B.” According to cluster analysis, the anticipated heterozygosity (gene diversity) ofNei (1973) was 0.591 on average. In summary, SSR markers successfully evaluated the genetic relationships among the sweetpotato accessions used and generated a high level of polymorphism. The results of the present study will be useful for themanagement of germplasm, improvement of the current breeding strategies, and the release of new cultivars as varieties.     

Biochemical association between the prevalence of genetic polymorphism and myocardial infarction

Genetic polymorphism has a vital role in the pathogenesis and development of myocardial infarction (MI). Single nucleotide polymorphism at any one of the amino acid sequences can result in a diseased state. A single gene can exhibit genetic polymorphism at more than one position giving rise to different variants. Genetic polymorphism of angiotensinogen (AGT) M235T, AGT T174M, and angiotensin-1-converting enzyme (ACE) I/D, endothelial nitric oxide synthase (eNOS), and methylenetetrahydrofolate reductase (MTHFR) can be a risk factor for MI. However, it is important to study the prevalence of genetic polymorphisms of these genes among different populations. MI is influenced by genetic polymorphism of various genes, including AGT, ACE, eNOS, MTHFR, etc. However, the association of genetic polymorphism of these genes varies among different populations, but different ethnic groups could show contradictory results. These genes have shown a positive association with risks of MI in some populations, whereas the results have not been consistent with every ethnic group. In this article, we have summarized the genetic variations in the aforementioned genes and their association with MI.