ABSTRACT
Since the outbreak of the COVID-19 pandemic, it has been suspected that its causative agent, the SARS-CoV-2 coronavirus, may cause transient or permanent hyperglycemia. This fact has resulted in a new focus of research interest related to the study of potential mechanisms leading to damage of pancreatic insulin-producing cells, as well as the possible impact of the virus on insulin sensitivity, which may manifest as metabolic disturbances in patients with COVID-19 and cause diabetes mellitus. Evidence from the literature suggests that Corona viruses can damage pancreatic (beta-cells by direct or indirect mechanisms and cause changes in insulin secretion and sensitivity. To what extent all these changes are valid claims that SARS-CoV-2 can trigger diabetes mellitus is still not fully proven.Copyright © 2022 Medical Information Center. All rights reserved.
ABSTRACT
Background COVID-19 as a trigger for A-beta+ ketosis-prone diabetes (KPD) [1,2] in previously normoglycemic individuals presenting with new-onset DKA, has been sparsely studied. Aim To study prospective changes in insulin secretion and insulin resistance in suspected A-beta+ KPD patients presenting with COVID-associated new-onset DKA. Method 22 previously non-diabetic, antibody-negative patients with new-onset DKA and RT-PCR positive COVID-19 (suspected A-beta + KPD), were followed up for one year. They were compared with 20 Type 1A and 18 Type 2 DM patients, with serial assessments (0,6 and 12 months) of insulin secretion rates (ISR) and multi-tissue insulin resistance (IR). 75-g OGTT with serial glucose, insulin and C-peptide estimation (0,15, 30,45, 60,90,120, 150 and 180 minutes) was used to derive IS, while hepatic and peripheral IR was calculated based on study by Ghani et al. [3]. Results At baseline, ISR in suspected KPD (n = 22) was significantly reduced but similar to Type 1A DM(p = 0.15). Serial ISR demonstrated complete recovery in 17 (77%) patients who became insulin independent at one-year follow-up (remission), while 5(23%) patients continued to require insulin (non-remission). KPD patients showed significant hepatic and peripheral IR at baseline compared to Type 1A DM (p < 0.05). The remission group (n = 17) showed significantly enhanced recovery of hepatic and peripheral insulin sensitivity at 6 and 12 months follow-up (all p < 0.01) compared to the non-remission (n = 5) group, with IR in the latter being comparable to Type 2 DM at follow-up (all p > 0.05). Younger age, lower BMI, initial severity of DKA and inflammation (IL-6 levels), along-with reduced 25-hydroxy-Vitamin-D levels were factors associated with poorer recovery of beta-cell secretion amongst the KPD patients. Conclusion This is the first prospective study to demonstrate progressive recovery of p-cell secretion in new-onset A-beta + KPD provoked by COVID-19 infection in Indian adults, with a distinctly different profile from Type 1A DM.Copyright © 2023 Elsevier B.V.
ABSTRACT
Since the outbreak of the COVID-19 pandemic, it has been suspected that its causative agent, the SARS-CoV-2 coronavirus, may cause transient or permanent hyperglycemia. This fact has resulted in a new focus of research interest related to the study of potential mechanisms leading to damage of pancreatic insulin-producing cells, as well as the possible impact of the virus on insulin sensitivity, which may manifest as metabolic disturbances in patients with COVID-19 and cause diabetes mellitus. Evidence from the literature suggests that Corona viruses can damage pancreatic (beta-cells by direct or indirect mechanisms and cause changes in insulin secretion and sensitivity. To what extent all these changes are valid claims that SARS-CoV-2 can trigger diabetes mellitus is still not fully proven.Copyright © 2022 Medical Information Center. All rights reserved.
ABSTRACT
Since the outbreak of the COVID-19 pandemic, it has been suspected that its causative agent, the SARS-CoV-2 coronavirus, may cause transient or permanent hyperglycemia. This fact has resulted in a new focus of research interest related to the study of potential mechanisms leading to damage of pancreatic insulin-producing cells, as well as the possible impact of the virus on insulin sensitivity, which may manifest as metabolic disturbances in patients with COVID-19 and cause diabetes mellitus. Evidence from the literature suggests that Corona viruses can damage pancreatic (beta-cells by direct or indirect mechanisms and cause changes in insulin secretion and sensitivity. To what extent all these changes are valid claims that SARS-CoV-2 can trigger diabetes mellitus is still not fully proven.Copyright © 2022 Medical Information Center. All rights reserved.
ABSTRACT
Introduction: Some patients with comorbidity such as diabetes are at risk of worsening after being infected with the COVID-19 and they usually adjust their diet during the recovery process. Aim: To explore the use of Stevia rebaudiana leaves as a natural sweetener recommended for COVID-19 patients and the nanoparticle approach of S. rebaudiana extract to improve the efficacy. Methods: Four electronic databases (Google Scholar, PubMed, Scopus, and ScienceDirect) were used with specified inclusion and exclusion criteria set. Results: The glycosides produced by S. rebaudiana are 300 times sweeter than sucrose, low in calories, and can control blood sugar levels and increase insulin secretion. The application of nanoparticles in S. rebaudiana extract is a new step to maximise efficacy, increase stability and solubility. Conclusion: S. rebaudiana can be used as an alternative diet for COVID-19 diabetes patients. The application of the nanoparticles can increase the stability and solubility, thus improving the efficacy.
ABSTRACT
Introduction: COVID-19 has been linked to an increased risk of new-onset diabetes mellitus and increased incidence of diabetic ketoacidosis (DKA) either as a new presentation or with pre-existing diabetes. Various mechanisms such as impaired insulin secretion, impaired glucose disposal or increased counter regulatory responses are proposed.2 Case report: A 57-year-old man diagnosed with COVID-19 one month prior presented with epigastric pain, shortness of breath and weight loss. Investigations confirmed DKA (pH 7.22, bicarbonate 2.6 mmol/L, blood glucose 11.6 mmol/L, blood ketones 5.8 mmol/L) with HbA1c of 95 mmol/mol. Initial treatment was started as per national DKA guidelines. Upon discharge, the patient was prescribed a basal-bolus regime (total 30 units of insulin) and a FreeStyle Libre flash glucose monitoring (FGM) device. Rapid improvement in blood glucose levels was observed, with regular down titration of insulin and complete discontinuation after 24 days. HbA1c was 37 mmol/mol 96 days later. C-peptide normalised at 3 months for paired glucose at 837 pmol/L. Discussion: The use of diabetes technology (FGM device) with remote monitoring of blood glucose was instrumental in the safe and effective management of this patient. Given that the available literature suggests transient beta-cell dysfunction in the majority of COVID-19 patients resulting in DKA,3 we propose that patients who have been diagnosed with COVID-19 presenting with DKA should be discharged with insulin and FGM from secondary care. This enables remote insulin titration with ease, de-escalation of treatment with confidence and avoiding hypoglycaemia in the recovery phase of the illness in those with transient beta-cell dysfunction due to COVID-19.
ABSTRACT
Background: Obesity is a major risk factor for the development of type 2 diabetes mellitus (T2DM). Post COVID-19 with an increased rate of obesity, there is a growing need for treatments providing improved efficacy and compliance. Modulation of nerves innervating organs that regulate plasma glucose (PG) may be a novel method for treating T2DM. Standalone stimulation of the vagus nerve or vagotomy/treatments has mixed/undesirable results. Long term/4 hrs dual neuromodulation consisting of simulation of celiac fibers innervating the pancreas (increasing insulin release) w/ simultaneous reversible electrical blockade of neuronal hepatic fibers innervating the liver (preventing glucose release) in obese T2DM animal models enhanced glycemic control superior to standalone treatments. This long term neuromodulation requires considerable amount of energy. Here we tested if glycemic control could be preserved w/ intermittent short-term neuromodulation. Methods: We used a proprietary bio-electronic device & algorithm developed by ReShape Lifesciences Inc. comprising Stimulation (Stim) of the celiac nerve w/ a simultaneous reversible high frequency alternating current (HFAC)-induced blockade of the hepatic nerve. Experiments were conducted in an Alloxan treated swine model of T2DM. Area under the curve (area units = AU) of Oral Glucose Tolerance Tests (OGTTs) was used to quantify glycemic control. Results: 30 min of HFAC/Stim @ OGTT initiation increased glycemic control (Sham = 6711 ± 1442 AU, HFAC/Stim = 545 ± 1632 AU, p < 0.05). During OGTT in Sham there was a 36 ± 7 mg/dL & 35 ± 9 mg/dL increase in PG @ 30 & 60 min w/ 9 ± 9 mg/dL @ 4 hrs. W/ 30 min of HFAC/Stim the PG was -5 ± 11 mg/dL & 3 ± 20 mg/dL relative to baseline @ 30 & 60 min & -7 ± 8 mg/dL @ 4 hrs. Interestingly, fasting PG remained suppressed by 34 ± 7 mg/dL following cessation of HFAC/Stim for 48 hrs. Histopathology demonstrated healthy tissues. Conclusions: These studies suggest a novel, reversible & intermittent energy efficient neuromodulation for the treatment of T2DM.