Prevalence and determinants of psychological insulin resistance among type 2 diabetic patients in Kinshasa, Democratic Republic of Congo

Background: Psychological insulin resistance (PIR) is a common but unappreciated phenomenon by health care providers with a negative impact on the control of type 2 diabetes mellitus. Aim: To determine the frequency of PIR and its determinants in patients with type 2 diabetes. Setting: This study was conducted in Kinshasa in three health centres providing management of diabetic patients. Methods: This study was a multicentric, cross-sectional study conducted from 01 November 2017 to 31 March 2018 in Kinshasa among 213 type 2 diabetic patients who were taking oral anti-diabetic drugs. A standardised questionnaire, the Chinese Attitudes to Starting Insulin Questionnaire (Ch-ASIQ), was used for data collection. Results: The average age of participants was 59.8 ± 11.1 years with a male to female ratio of 1.5. The prevalence of PIR was 42.7%; and its main determinants were 50 years of age (odds ratios [OR] adjusted 2.05; 95% confidence interval [CI] 1.98­4.27; p = 0.045), the presence of complications (OR adjusted 3.33; 95% CI 1.68­6.60; p = 0.001), lack of knowledge about insulin therapy (OR adjusted 1.96; 95% CI 1.03­3.71; p = 0.040) and the high cost of insulin (OR adjusted 2.32; 95% CI 1.08­4.95; p = 0.030).Conclusion: The study showed that almost half of type 2 diabetic patients had PIR with the main determinant factors related to the patient and the health system. The establishment of a therapeutic education programme, improved 'provider­patient' communication and the development of approaches to increase access to drugs are crucial to reduce the prevalence of PIR

The relationship between vitamin D deficiency and NAFLD in sample of Egyptian type 2 diabetic patients

Background: vitamin D deficiency has a strong association with insulin resistance and NAFLD.Objective: to assess vitamin D levels in patients having type2 diabetes with NAFLD and to study its relationship withinsulin resistance. Patients and methods: a case­control study conducted on 50 subjects who were divided into 2 groups: 35 patients having T2DM and NAFLD (group 1) and 15 healthy subjects served as control (group 2). Fasting plasma glucose (FBG), 2 hour post prandial (2hrpp), and fasting plasma insulin (FPI) were measured with calculation of HOMA-IR. Fasting lipids, Hb A1c, calcium, phosphorus, urea, creatinine, serum alanine aminotranseferase (ALT), aspartate aminotransaminase (AST) were also measured. BMI was calculated, serum 25 (OH)D was measured with ELISA and abdominal ultrasonography was done for all participant. Results: the study showed lower level of vitamin D in patients with T2DM and NAFLD 10.6 (5.5-21.3) as compared to control group 31 (27-39.7). While non-significant difference was found between male and female regarding 25(OH) D level and HOMA-IR. There was significant negative correlation between vitamin D level and HOMA-IR. Conclusion: Vitamin D level was associated with presence of NAFLD. There was strong relation between vitamin D level and insulin resistance as vitamin D deficiency was associated with higher levels of HOMA-IR. Obesity may be related to low vitamin D level, but no difference in VD level between males and females was found

Insulin resistance in apparently healthy adult nigerians: association with magnesium status

Magnesium plays a critical role in glucose metabolism and evidences suggest that magnesium deficiency is associated with decreased insulin sensitivity. However, it is likely that these relationships are affected by genetic and environmental factors that can differ among different populations. The aim of this study was to determine the prevalence of insulin resistance and its association with magnesium status among apparently healthy adult Nigerians. Fasting plasma levels of magnesium, glucose and insulin were determined in 120 apparently healthy adults. Insulin resistance was calculated as HOMA-IR. Prevalence of insulin resistance was estimated and the association between plasma magnesium levels and HOMA-IR was determined. About 19.2% of the study subjects were classified as having insulin resistance. Prevalence was higher among males compared to females (21.0% vs. 17.0%) and among obese compared to normal weight subjects (26.1% vs. 14.9%). Subjects with hypomagnesemia had higher prevalence of insulin resistance compared with subjects who had normal plasma magnesium levels (50.0% vs. 14.4%). Insulin resistance was inversely associated with plasma magnesium level independent of age, gender and BMI. Insulin resistance is relatively common among apparently healthy individuals in this study. Magnesium deficiency was found to be a significant predictor of insulin resistance. We recommend further studies that will investigate whether optimization of magnesium status in general population or among individuals at risk of developing type 2 diabetes will be a useful approach in lowering insulin resistance and prevent or delay onset of type 2 diabetes mellitus in our setting

Vitamin D supplementation improves insulin resistance in type 2 diabetes subjects in Lagos, Nigeria

Type 2 diabetes is a disease caused by both insulin resistance and an insulin secretory defect. Reports suggest that vitamin D3 supplementation improves insulin resistance and pancreatic beta-cell function, but there is paucity of data on vitamin D and glycaemia in type 2 diabetes in Nigeria. We have therefore performed a single blind prospective randomised placebo-controlled trial, involving type 2 diabetes participants in Lagos, Nigeria. The participants consisted of 42 type 2 diabetes patients with vitamin D deficiency. These participants were randomised into two equal groups of treatment and a placebo arm. Vitamin D3(3000 IU daily) was given to the participants in the treatment arm. Insulin resistance (HOMA-IR) and pancreatic beta-cell (HOMA-B) function were determined at baseline and after 12 weeks of vitamin D3 supplementation, or placebo treatment. There was a reduction from baseline in the mean insulin resistance level in both the treatment and placebo groups. How-ever, this reduction was only statistically significant in the treatment group (p <0.01). The proportion of subjects with improvement in insulin resistance status (homeostatic model assessment insulin resistance score (HOMA-IR)<2.0) was significantly higher in the treatment arm (p<0.05). There was a reduction in the mean insulin secretory capacity in the treatment group while it increased in the placebo group, though this difference was not statistically significant. We conclude that vitamin D3 supplementation results in a reduction in insulin resistance, but has no effect on pancreatic beta-cell function in type 2 diabetes

Vitamin D Levels and Insulin Resistance among Nigerian men with Type-2 Diabetes mellitus

Background: A number of studies have shown a high prevalence of insufficient vitamin D levels in humans in the North American, European and Asian regions. Various research works have also shown that low serum vitamin D levels play a major role in the pathogenesis of chronic, non-infective illnesses such as diabetes mellitus and cancer.Objective: This study was aimed at assessing the serum vitamin D status in relation to glucose homeostasis among men with Type-2 Diabetes mellitus and normal controls.Methods: This comparative cross-sectional study included 80 men with confirmed diagnosis of Type-2 diabetes mellitus and 49 normal adult male controls. Serum 25-hydroxy vitamin D, fasting serum C-peptide and fasting plasma glucose levels were measured in both study groups.Results: There was a significant difference between the mean serum 25-OH vitamin D levels among the cases (36.55ng/mL) and the controls (42.96ng/mL) (p = 0.001). All the four 25-OH vitamin D-deficient subjects had diabetes. In the diabetes group, 43.8% had a normal insulin resistance compared to 61.8% of the control group (p = 0.054). In the diabetes group, 73.8% had sufficient vitamin D, 21.2% had insufficient vitamin D and 5% had vitamin D deficiency. In the control group, there was a significant negative correlation between serum 25-OH vitamin D and BMI and fasting plasma glucose. The mean HOMA2IR value for the diabetes group (3.09) was higher than the value for the controls (2.40).Conclusion: The mean serum 25-OH vitamin D level in the diabetes group was lower than that of the control group hence, hypovitaminosis D may be a contributor to the onset of diabetes mellitus among Nigerian men

Glycaemic Control and Cardiovascular Outcomes in Diabetes : Review

While type 1 diabetes mellitus (DM) is characterised by insulin deficiency due to pancreatic beta-cell destruction; type 2 DM is characterised by a state of longstanding insulin resistance (IR); compensatory hyperinsulinaemia and varying degrees of elevated plasma glucose levels (PG); associated with clustering of cardiovascular (CV) risk and the development of macrovascular disease prior to the diagnosis of DM. Coronary artery disease (CAD) accounts for 70of mortality and morbidity in patients with diabetes. Studies in diabetes care have helped prevent or reduce microvascular complications in type 1 and 2 diabetes. However the same cannot be said about macrovascular disease. Despite all data concerning the association between diabetes and cardiovascular disease (CVD); the exact mechanism by which diabetes is linked to atherosclerosis is incompletely understood; and this is especially true in the case of hyperglycaemia. The positive effect of intensive glucose management in comparison to non-intensive glucose control is far from proven. The DCCT and UKPDS studies have shown that while glycaemic control is important for preventing long-term macrovascular complications; early glucose control is far more rewarding (metabolic memory). Later trials such as ACCORD; ADVANCE and VADT do not advocate tight glycaemic control. In fact; the ACCORD trial has shown increased mortality with tight glucose control. Tight glucose control may be beneficial in selected patients with short disease duration; long life expectancy and no CVD. In critically ill patients; a blood glucose target of 140-180 mg is fairly reasonable and achievable. The ESC/EASD guidelines of October 2013; like those of the ADA; AHA and ACC; continue to endorse a treatment target for glucose control in diabetes of HbAlc level 7; based predominantly on microvascular disease with acknowledged uncertainty regarding the effect of the intensive glucose control on CVD risk. Management of hyperglycaemia in diabetics should not be considered in isolation; diabetics require multifactorial intervention for hypertension; dyslipidaemia and microalbuminuria besides hyperglycaemia. In fact; the combined use of antihypertensives; aspirin and lipid-lowering agents makes it difficult to discern the beneficial effects of antihyperglycaemic therapy

Diabetes Mellitus and the Brain : Special Emphasis on Cognitive Function : Review

Diabetes mellitus (DM) is a major public health problem. Cognitive deficits are common with DM which range from subclinical or subtle to severe deficits such as dementia. Both hypoglycaemia and hyperglycaemia are causes of cognitive impairment with DM. In patients with DM; not only severe hypoglycaemia but also recurrent mild or moderate hypoglyacemia have deleterious effect on the brain. Recurrent mild/moderate hypoglycaemia is associated with intellectual decline; reduced attention; impaired mental abilities and memory deficits. Hypoglycaemia may result in abnormalities of neuronal plasticity; synaptic weakening and scattered neuronal death in the cerebral cortex and hippocampus. Chronic hyperglycaemia in type 1 and type 2 DM is associated with low IQ (verbal; performance and total) and abnormalities in testing for different domains of cognitive function such as verbal relations; comprehension; visual reasoning; pattern analysis; quantitation; memory; learning; mental control; psychomotor efficiency; mental and motor processing speed and executive function. The suggested mechanisms incriminated in the pathogenesis of hyperglycaemia-related cognitive dysfunction include; macro- and microvascular disease or vasculopathy; hyperlipidaemia; hypertension; insulin resistance and hyperinsulinaemia; stress response; direct toxic effect of chronic hyperglycaemia on the brain; advanced glycation end-products; inflammatory cytokines and oxidative stress. Hyperglycaemia causes oxidative stress; amyloidosis; angiopathy; abnormal lipid peroxidation; accumulation of ?-amyloid and tau phosphorylation; neuro-inflammation; mitochondrial pathology; apoptosis and neuronal degeneration in the cortex and hippocampus. Depression has been identified as a risk for accelerated cognitive decline with DM. The knowledge that diagnosis at an early age; frequency of hypoglycaemia; poor glycaemic control and presence of risk factors negatively affect cognitive functions in DM will have important implications for treatment and research purposes

Insulin Resistance Induced by Antiretroviral Drugs: Current Understanding of Molecular Mechanisms

The increase in incidence of HIV infection continues to be a major public health problem across the world; but more especially in sub- Saharan Africa. Treatment with highly active antiretroviral therapy (HAART) has improved the prognosis of patients with AIDS; but it has also increased the incidence of various metabolic disorders; in particular insulin resistance accompanied by dyslipidaemia; hyperglycaemia and lipodystrophy. This is often accompanied by frank type 2 diabetes and increased mortality from cardiovascular disease. It is important to understand the mechanistic basis for these side-effects as the incidence of these is likely to increase as the rollout of antiretroviral drugs continues

Serum Resistin Levels in Nonalcoholic Fatty Liver Disease and their Relationship to Severity of Liver Disease

Background: Resistin is a hormone that is linked to the development of insulin resistance (IR); but information on the direct relationship of resistin levels in humans with nonalcoholic fatty liver disease (NAFLD); and their effect on the histological severity of NAFLD; is lacking. Objective: The aim of the current study is to determine the circulating resistin levels obtained from patients with NAFLD and to correlate them with insulin resistance and hepatic histological features. Methods: Blood samples were collected from 30 consecutive patients with liver-biopsy-proven NAFLD and 30 subjects as controls. Serum resistin levels were measured. Body mass index (BMI) was calculated for all subjects; and serum insulin; C-peptide; and lipoprotein levels were also measured. Results: Mean serum resistin level and BMI in the NAFLD group were significantly higher than in the controls (both P 0.001). Both men and women in the NAFLD group had higher mean serum resistin levels than did the men and women in the control group (all P 0.001). Multivariate analysis showed that the percentage of hepatic steatosis; sex; BMI; and homeostasis model assessment of insulin resistance [HOMA(IR)] were related to serum resistin levels. Conclusion: These data suggest increased resistin levels in NAFLD patients which are related to histological severity of the disease. These findings support the link between resistin; insulin resistance and BMI in these patients

Insulin Resistance: Causes and Metabolic Implications

Insulin is an anabolic hormone that plays key roles in glucose metabolism. Insulin resistance is a decreased biological response to normal concentration of circulating insulin. In insulin resistance; normal amounts of insulin are inadequate to produce a normal insulin response from fat; muscle and liver cells. Insulin resistance in fat cells results in hydrolysis of stored triglycerides; which elevates free fatty acids in the blood plasma. In muscles; it reduces glucose uptake; whereas in the liver; it reduces glucose storage with both effects serving to elevate blood glucose. High plasma levels of Insulin and glucose due to Insulin resistance often lead to metabolic syndrome and type 2 diabetes mellitus. The cause of the vast majority of cases of insulin resistance remains unknown. However; it is claimed that insulin resistance might be caused by a high carbohydrate diet. Studies have shown that glucosamine (often prescribed for joint problems) may cause Insulin resistance. It is also reported that insulin resistance occurrence in a population increased as sugar consumption and addition of high fructose corn syrup to diets increased. Physical inactivity and obesity have been implicated as factors; which aggravate insulin resistance. The presumption that a defect in specific gene may cause insulin resistance is still under investigation

Diabetes: Part 1. Definition; Diagnosis and Prevention

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Adiponectin

Adipose tissue is not considered anymore as a passive depot for storing excess energy in the form of triglycerides but as an active organ secreting several hormones or adipokines. This review gives some knowledge about history of discovery; ways of measurements; and biochemical and pathophysiological effects of adiponectin

Abnormal Cation Exchange in Insulin-Resistant Patients with Essential Hypertension : Cardiovascular Topics

Objectives: To identify important factors that may contribute to abnormal glucose tolerance in elderly patients with treated hypertension with primary reference to changes in the following parameters: calculated insulin resistance; endogenous insulin processing and secretion; platelet cation concentration and membrane ATPase activity. Design: Thirty-nine patients receiving antihypertensive therapy (including low-dose thiazide treatment) were compared to 13 normotensive; normoglycaemic control subjects. Total platelet cation concentration and membrane ATPase activity were measured and; following a 75-g oral glucose test; serum insulin; proinsulin and 31-32 des-proinsulin responses were measured in prospectively defined hypertensive patients with normal glucose tolerance (NG); impaired glucose tolerance (iGT) and diabetes mellitus (DM). Results: of the total patient cohort; seven patients manifested newly diagnosed DM; 18 had iGT and 14 NG. Among the three groups; no difference in duration of drug use (thiazides and beta-blockers) was noted; BMi and waist-to-hip ratio increased progressively from NG to iGT to overt DM. Compared to NG patients; serum insulin responses were significantly greater in the iGT (all time points) and DM (two-hour measurements) subjects. Proinsulin and 31-32 des-proinsulin serum responses were likewise significantly higher in the iGT and DM groups. The derived measure of insulin resistance in the hypertensive patients showed a significant increase in the progression from NG to iGT and DM. Mean total platelet potassium concentration was reduced in the DM compared to the iGT and the control groups; while platelet sodium; calcium and magnesium concentrations showed no Significant differences. Platelet membrane magnesium ATPase activity was significantly higher in the normotensive control versus the hypertensive group. Sodium; potassium and calcium ATPase activity showed no significant differences among the subgroups. Conclusion: our findings support the strong link between essential hypertension; insulin resistance / hyperinsulinaemia and regional adiposity. Beta-cell dysfunction (hypersecretion and abnormal insulin processing) is manifest in the progression from normality to overt diabetes. The use of antihypertensive therapy (low-dose thiazides and cardioselective beta-blockers) possibly added diabetogenic effect(s). The reduction in platelet total potassium concentration paralleled the diabetic state while a reduced membrane magnesium ATPase activity correlated with the hypertensive state