Carbohydrates play an important role in blood glucose control in pregnant women with GDM. Carbohydrate-restricted dietary (CRD) pattern for gestational diabetes mellitus (GDM) has been widely used in clinics, but the change in insulin utilization rate beyond CRD intervention in GDM remains unclear. The aim of the present study was to explore the application of insulin in pregnancy with GDM, as well as the influence of CRD pattern on lipid metabolism and nutritional state. A retrospective study of 265 women with GDM who delivered in Peking University People’s Hospital from July 2018 to January 2020 was conducted using a questionnaire survey. Women were divided into a CRD group or a control group according to whether they had received CRD intervention during pregnancy. There was no statistically significant difference in the rate of insulin therapy between the two groups (p > 0.05), the initial gestational week of the CRD group combined with insulin treatment was significantly higher than that of the control group (p < 0.05), and the risk of insulin therapy was positively correlated with fasting plasma glucose (FPG) in early pregnancy (p < 0.05). The incidence of abnormal low-density lipoprotein cholesterol levels in the CRD group was significantly lower than that in the control group (p < 0.05). There were no significant differences in nutritional indexes between the two groups. The results indicate that CRD intervention may be effective in delaying the use of insulin and improving the blood lipids metabolism during GDM pregnancy, while nutritional status may not be significantly affected under CRD intervention, and a high FPG in early pregnancy with GDM may be a risk factor for combined insulin therapy with CRD intervention.
Gestational diabetes mellitus (GDM) is associated with hypertensive disorders in pregnancy. Alpha-methyl-DOPA (αMD) is a commonly used medication for hypertension in pregnant women. This medication may be associated with alteration in insulin resistance and glucose homeostasis. The aim of the present study was to investigate in 152 pregnant women whether the demands of exogenous insulin in glucocorticoid-treated women during pregnancy are different between those with GDM and hypertension treated with αMD and those without hypertension. In the group of women with GDM under insulin treatment, who received αMD for hypertension, the increase in insulin needs was relatively lower by at least 30% of the pre-admission insulin dose compared to all of the remaining women not receiving αMD in the same group (9 women vs. 50 women, p = 0.035). Our work raises the hypothesis that αMD can favorably modulate insulin sensitivity in the third trimester of pregnancy in previously insulin-treated women with gestational diabetes who receive glucocorticoids.
The discharge from hospital of insulin-treated hyperglycemic patients is always challenging. This is even more so in patients requiring glucocorticoid treatment, such as those with COVID-19.
Patients and method:
A retrospective monocentric study of 23 inpatients with newly diagnosed or already known diabetes mellitus (DM) who were naïve to insulin treatment, , and who were hospitalized with COVID-19 in non-critical settings and then discharged. Patients were followed-up for one month after discharge for the management of insulin treatment by a multi-professional team through phone consultations.
Insulin prescriptions at discharge were 24.6 ± 14 U/day injected in 2 ± 1.5 daily shots. A mean of three phone consultations were required. One month later, the mean insulin reduction was 1.5 ± 1.3 shots and 6 ± 5 U/day. All patients reached their glycemic target without hypoglycemic events, drop-outs, or readmissions.
This study demonstrates the feasibility, efficacy, and safety of a multi-professional approach through telemedicine for managing DM patients after discharge during COVID-19.
Lately, an increasing number of studies have investigated the relationship between metformin and gut microbiota, suggesting that metformin exerts part of its hypoglycemic effect through the microbes. However, its underlying mechanism remains largely undetermined. In the present study, we investigated the effects of metformin on gut microbiota and metabolome profiles in serum and compared it with insulin treatment in rats with type 2 diabetes mellitus (T2DM). Diabetic rats (DM group) were induced by a combination of streptozotocin and high-fat diet (HFD). After 7 days, DM rats were treated with metformin (MET group) or insulin (INS group) for 3 weeks. The 16S rRNA sequencing of the gut microbiota and non-targeted metabolomics analysis of serum were conducted. A total of 13 bile acids (BAs) in serum were further determined and compared among different groups. The rat model of T2DM was well established with the typical diabetic symptoms, showing significantly increased blood glucose, AUC of OGTT, HOMA-IR, TC, TG, LDL-C and TBA. Metformin or insulin treatment could ameliorate symptoms of diabetes and partly recover the abnormal biochemical indicators. Compared with DM rats, the relative abundances of 13 genera were significantly changed after metformin treatment, while only three genera were changed after insulin treatment. The metformin and insulin treatments also exhibited different serum metabolome profiles in T2DM rats. Moreover, 64 differential metabolites were identified between MET and DM groups, whereas 206 were identified between INS and DM groups. Insulin treatment showed greater influence on amino acids, glycerophospholipids/glycerolipids, and acylcarnitine compared with the metformin treatment, while metformin had an important impact on BAs. Furthermore, metformin could significantly decrease the serum levels of CA, GCA, UDCA, and GUDCA, but increase the level of TLCA in DM rats. Insulin treatment significantly decreased the levels of CA, UDCA, and CDCA. Besides, several metabolites in serum or microbiota were positively or negatively correlated with some bacteria. Collectively, our findings indicated that metformin had a stronger effect on gut microbiota than insulin, while insulin treatment showed greater influence on serum metabolites, which provided novel insights into the therapeutic effects of metformin on diabetes.
The year 2021 is the centennial of insulin discovery. The discovery of insulin changes diabetes mellitus from a death sentence to a manageable disease. It became a historical turning point in the lives of people with diabetes. Since the first use of insulin in a patient in 1922, insulin and its analogs have been remarkable in saving the lives of people with diabetes. As insulin began to be used as a drug, it was introduced to, and used in Korea until now. This review briefly summarizes the history of insulin treatment in Korean children and adolescents with diabetes.
Aim. To evaluate clinical characteristics and perinatal outcomes in a heterogeneous population of Caucasians born in Italy and High Migration Pressure Countries (HMPC) women with GDM living in Piedmont, North Italy. Methods. We retrospectively analyzed data from 586 women referring to our unit (2015–2020). Epidemiological (age and country of origin) and clinical-metabolic features (height, weight, family history of DM, parity, previous history of GDM, OGTT results, and GDM treatment) were collected. The database of certificates of care at delivery was consulted in relation to neonatal/maternal complications (rates of caesarean sections, APGAR score, fetal malformations, and neonatal anthropometry). Results. 43.2% of women came from HMPC; they were younger
and required insulin treatment more frequently than Caucasian women born in Italy (χ2 = 17.8,
). Higher fasting and 120-minute OGTT levels and gestational BMI increased the risk of insulin treatment (OGTT T0: OR = 1.04, CI 95% 1.016–1.060,
; OGTT T120: OR = 1.01, CI 95% 1.002–1.020,
; BMI: OR = 1.089, CI 95% 1.051–1.129,
). Moreover, two or more diagnostic OGTT glucose levels doubled the risk of insulin therapy (OR = 2.03, IC 95% 1.145–3.612,
). We did not find any association between ethnicities and neonatal/maternal complications. Conclusions. In our multiethnic GDM population, the need for intensive care and insulin treatment is high in HPMC women although the frequency of adverse peripartum and newborn outcomes does not vary among ethnic groups. The need for insulin therapy should be related to different genetic backgrounds, dietary habits, and Nutrition Transition phenomena. Thus, nutritional intervention and insulin treatment need to be tailored.
This paper examines the evidence behind the use and decline of insulin coma therapy as a treatment for schizophrenia and how this was viewed by the psychiatric profession. The paper demonstrates that, from the time of its introduction, there was considerable debate regarding the evidence for insulin treatment, and scepticism about its purported benefits. The randomized trials conducted in the 1950s were the result, rather than the origins, of this debate. Although insulin treatment was subsequently abandoned, it was still regarded as a historic moment in the modernization of psychiatry. Then, as now, evidence does not speak for itself, and insulin continued to be incorporated into the story of psychiatric progress even after it was shown to be ineffective.
β-Amyloid precursor protein-cleaving enzyme-1 (BACE1) initiates the
production of Aβ-peptides that form Aβ-plaque in Alzheimer’s disease.
Reportedly, acute insulin treatment in normal mice, and hyperinsulinemia in high-fat-fed
(HFF) obese/diabetic mice, increase BACE1 activity and levels of Aβ-peptides and phospho-
-thr-231-tau in the brain; moreover, these effects are blocked by PKC-λ/ι inhibitors. However, as
chemical inhibitors may affect unsuspected targets, we presently used knockout methodology to
further examine PKC-λ/ι requirements. We found that total-body heterozygous PKC-λ knockout reduced acute stimulatory effects of insulin and chronic effects of hyperinsulinemia in HFF/obese/diabetic mice, on brain PKC-λ activity and production of Aβ1-40/42 and phospho-thr-231-tau. This protection in HFF mice may reflect that hepatic PKC-λ haploinsufficiency prevents the development
of glucose intolerance and hyperinsulinemia.
On the other hand, heterozygous knockout of PKC-λ markedly reduced brain levels of
BACE1 protein and mRNA, and this may reflect diminished activation of nuclear factor kappa-B
(NFκB), which is activated by PKC-λ and increases BACE1 and proinflammatory cytokine transcription. Accordingly, whereas intravenous administration of aPKC inhibitor diminished aPKC activity and BACE1 levels by 50% in the brain and 90% in the liver, nasally-administered inhibitor
reduced aPKC activity and BACE1 mRNA and protein levels by 50-70% in the brain while sparing
the liver. Additionally, 24-hour insulin treatment in cultured human-derived neurons increased
NFκB activity and BACE1 levels, and these effects were blocked by various PKC-λ/ι inhibitors.
PKC-λ/ι controls NFκB activity and BACE1 expression; PKC-λ/ι inhibitors may be
used nasally to target brain PKC-λ/ι or systemically to block both liver and brain PKC-λ/ι, to regulate NFκB-dependent BACE1 and proinflammatory cytokine expression.