1.
Targeting the Adipose Tissue in COVID-19.
Malavazos, AE, Corsi Romanelli, MM, Bandera, F, Iacobellis, G
Obesity (Silver Spring, Md.). 2020;28(7):1178-1179
-
-
Free full text
-
Plain language summary
A UK study showed that 72% of COVID-19 patients in critical care units had either overweight or obesity, whilst studies in Italy have shown that 99% of deaths occurred in patients who had at least one underlying chronic condition, including obesity, diabetes and hypertension. As obesity is tightly connected with diabetes and other inflammatory conditions, it is difficult to separate the effects of the obesity per se, from other chronic conditions that are commonly associated with the obesity. The authors discuss possible molecular mechanisms by which the fat tissue itself may increase the risk of more severe COVID-19 disease, such as angiotensin converting enzyme 2 (ACE2) receptors and dipeptidyl peptidase 4 (two receptors which occur in fat tissue and may be entry points of the virus into the cell) and an imbalance between the secretion of anti‐ and proinflammatory compounds from visceral fat cells. The authors conclude that the role of the adipose (fat) tissue during infectious diseases, such as COVID‐19, could be important and note that this is a modifiable risk factor.
2.
COVID-19 and diabetes: The why, the what and the how.
Cuschieri, S, Grech, S
Journal of diabetes and its complications. 2020;34(9):107637
-
-
-
Free full text
-
Plain language summary
Early reports have shown that individuals with diabetes who contract Covid-19 have higher hospital admissions and mortality rates, classing them as a vulnerable group. This review paper aimed to explain why this group of people are vulnerable and what measures could be recommended. The paper outlined that individuals with diabetes have a compromised immune system due to uncontrolled blood sugar levels. In addition to this, individuals with diabetes and Covid-19 may have a higher risk of organ damage due to the effects of the body's immune response combined with the disordered biological processes associated with their pre-existing condition. Conversely, it was discussed that Covid-19 could exacerbate diabetes progression if the Covid-19 virus entered the cells of the pancreas, causing a blood sugar imbalance. As a result, the importance of optimal blood sugar control was outlined. Several medications were addressed and their benefits/disadvantages discussed. Amongst those reviewed were medications such as GLP-1 agonists, which may help with controlling blood sugar levels and may prevent Covid-19 entering the body's own cells, and metformin, which was initially developed as an anti-influenza drug. Finally the paper discussed diabetes specific precautions to avoid contracting Covid-19. Vitamin D supplementation, regular blood sugar checks, lifestyle measures such as exercise and dietary requirements and allowing individuals with diabetes to have large supplies of their medications to avoid leaving the house were discussed. It was concluded that during the Covid-19 pandemic, individuals with diabetes require particular care in order to avoid additional burden on healthcare systems. For those individuals with diabetes who haven’t contracted Covid-19, this paper could be used to recommend any extra precautions to take to avoid contracting this virus.
Abstract
BACKGROUND The novel coronavirus SARS-CoV-2 has taken the world by storm. Alongside COVID-19, diabetes is a long-standing global epidemic. The diabetes population has been reported to suffer adverse outcomes if infected by COVID-19. The aim was to summarise information and resources available on diabetes and COVID-19, highlighting special measures that individuals with diabetes need to follow. METHODS A search using keywords "COVID-19" and "Diabetes" was performed using different sources, including PubMed and World Health Organization. RESULTS COVID-19 may enhance complications in individuals with diabetes through an imbalance in angiotension-converting enzyme 2 (ACE2) activation pathways leading to an inflammatory response. ACE2 imbalance in the pancreas causes acute β-cell dysfunction and a resultant hyperglycemic state. These individuals may be prone to worsened COVID-19 complications including vasculopathy, coagulopathy as well as psychological stress. Apart from general preventive measures, remaining hydrated, monitoring blood glucose regularly and monitoring ketone bodies in urine if on insulin is essential. All this while concurrently maintaining physical activity and a healthy diet. Different supporting entities are being set up to help this population. CONCLUSION COVID-19 is a top priority. It is important to remember that a substantial proportion of the world's population is affected by other co-morbidities such as diabetes. These require special attention during this pandemic to avoid adding on to the burden of countries' healthcare systems.
3.
Niacin Cures Systemic NAD+ Deficiency and Improves Muscle Performance in Adult-Onset Mitochondrial Myopathy.
Pirinen, E, Auranen, M, Khan, NA, Brilhante, V, Urho, N, Pessia, A, Hakkarainen, A, Kuula, J, Heinonen, U, Schmidt, MS, et al
Cell metabolism. 2020;31(6):1078-1090.e5
-
-
-
Free full text
Plain language summary
Nicotinamide adenine dinucleotide (NAD+) metabolite and its derivatives are fundamental orchestrators of daily homeostasis in our tissues. The relative amounts of NAD forms (NAD+, NADH, NADP, and NADPH) and their cofactor functions to drive metabolism to either catabolic or anabolic direction, deciding whether nutrients are broken down to synthesize ATP (adenosine 5′-triphosphate), the cellular energy currency or used as building blocks for growth and repair. An increased NAD+ /NADH ratio is a signal for a low nutrient state activating cellular fasting responses. The main question of this study was whether NAD+ levels are depleted in mitochondrial dysfunction, as mitochondria are regulating NAD+ concentrations, and if so, whether NAD+ deficiency can be restored in the tissues of the patients. Results show that mitochondrial muscle disease causes NAD+ deficiency, a myopathy-induced vitamin B3 deficiency, a metabolic pellagra. Furthermore, NAD+ levels can be rescued by a potent NAD+ booster niacin, a vitamin B3 form. Authors conclude that their findings (1) underscore the potent role of micronutrient vitamin B3 as a metabolic modifier; (2) identify NAD+ deficiency as a contributor to mitochondrial myopathy progression; (3) point to usefulness of niacin therapy for progressive external ophthalmoplegia patients; (4) introduce blood NAD+ test as a tool to identify and follow-up NAD+ deficiency; (5) indicate that correction of metabolome and function can occur without correction of transcriptional stress responses, emphasizing importance of metabolomic analysis in follow-up of treatment efficacy.
Abstract
NAD+ is a redox-active metabolite, the depletion of which has been proposed to promote aging and degenerative diseases in rodents. However, whether NAD+ depletion occurs in patients with degenerative disorders and whether NAD+ repletion improves their symptoms has remained open. Here, we report systemic NAD+ deficiency in adult-onset mitochondrial myopathy patients. We administered an increasing dose of NAD+-booster niacin, a vitamin B3 form (to 750-1,000 mg/day; clinicaltrials.govNCT03973203) for patients and their matched controls for 10 or 4 months, respectively. Blood NAD+ increased in all subjects, up to 8-fold, and muscle NAD+ of patients reached the level of their controls. Some patients showed anemia tendency, while muscle strength and mitochondrial biogenesis increased in all subjects. In patients, muscle metabolome shifted toward controls and liver fat decreased even 50%. Our evidence indicates that blood analysis is useful in identifying NAD+ deficiency and points niacin to be an efficient NAD+ booster for treating mitochondrial myopathy.