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Diabetes Research and Clinical Practice May 2017Postprandial hyperglycemia plays a decisive role in the development of chronic metabolic disorders. The effect of vinegar intake with a meal on postprandial glucose has... (Meta-Analysis)
Meta-Analysis Review
OBJECTIVE
Postprandial hyperglycemia plays a decisive role in the development of chronic metabolic disorders. The effect of vinegar intake with a meal on postprandial glucose has been studied in several trials with conflicting results.
RESEARCH METHODS AND PROCEDURES
The purpose of the current study was to systematically review control trials that report on the effect of vinegar intake on postprandial glucose response. Postprandial insulin response was considered as secondary outcome.
RESULTS
The pooled analysis of studies revealed a significant mean glucose and insulin area under the curve (AUC) reduction in participants who consumed vinegar compared with the control group (standard mean difference=-0.60, 95%CI -1.08 to -0.11, p=0.01 and -1.30, 95%CI -1.98 to -0.62, p<0.001, respectively).
CONCLUSIONS
The findings suggest that vinegar can be effective in reducing postprandial glucose and insulin levels, indicating it could be considered as an adjunctive tool for improving glycemic control.
Topics: Acetic Acid; Blood Glucose; Cross-Over Studies; Female; Humans; Hyperglycemia; Insulin; Male; Postprandial Period
PubMed: 28292654
DOI: 10.1016/j.diabres.2017.01.021 -
International Journal of Molecular... Nov 2022The prevalence of type 1 diabetes (T1D) is rising steadily. A potential contributor to the rise is vitamin D. In this systematic review, we examined the literature... (Review)
Review
The prevalence of type 1 diabetes (T1D) is rising steadily. A potential contributor to the rise is vitamin D. In this systematic review, we examined the literature around vitamin D and T1D. We identified 22 papers examining the role of vitamin D in cultured β-cell lines, islets, or perfused pancreas, and 28 papers examining vitamin D in humans or human islets. The literature reports strong associations between T1D and low circulating vitamin D. There is also high-level (systematic reviews, meta-analyses) evidence that adequate vitamin D status in early life reduces T1D risk. Several animal studies, particularly in NOD mice, show harm from D-deficiency and benefit in most studies from vitamin D treatment/supplementation. Short-term streptozotocin studies show a β-cell survival effect with supplementation. Human studies report associations between VDR polymorphisms and T1D risk and β-cell function, as assessed by C-peptide. In view of those outcomes, the variable results in human trials are generally disappointing. Most studies using 1,25D, the active form of vitamin D were ineffective. Similarly, studies using other forms of vitamin D were predominantly ineffective. However, it is interesting to note that all but one of the studies testing 25D reported benefit. Together, this suggests that maintenance of optimal circulating 25D levels may reduce the risk of T1D and that it may have potential for benefits in delaying the development of absolute or near-absolute C-peptide deficiency. Given the near-complete loss of β-cells by the time of clinical diagnosis, vitamin D is much less likely to be useful after disease-onset. However, given the very low toxicity of 25D, and the known benefits of preservation of C-peptide positivity for long-term complications risk, we recommend considering daily cholecalciferol supplementation in people with T1D and people at high risk of T1D, especially if they have vitamin D insufficiency.
Topics: Mice; Animals; Humans; Vitamin D; Diabetes Mellitus, Type 1; C-Peptide; Mice, Inbred NOD; Vitamins
PubMed: 36430915
DOI: 10.3390/ijms232214434 -
The American Journal of Clinical... Oct 2019Low-glycemic index (GI) diets are thought to reduce postprandial glycemia, resulting in more stable blood glucose concentrations. (Meta-Analysis)
Meta-Analysis
BACKGROUND
Low-glycemic index (GI) diets are thought to reduce postprandial glycemia, resulting in more stable blood glucose concentrations.
OBJECTIVE
We hypothesized that low-GI diets would be superior to other diet types in lowering measures of blood glucose control in people with type 1 or type 2 diabetes, or impaired glucose tolerance.
METHODS
We searched PubMed, the Cochrane Library, EMBASE, and clinical trials registries for published and unpublished studies up until 1 March, 2019. We included 54 randomized controlled trials in adults or children with impaired glucose tolerance, type 1 diabetes, or type 2 diabetes. Continuous data were synthesized using a random effects, inverse variance model, and presented as standardized mean differences with 95% CIs.
RESULTS
Low-GI diets were effective at reducing glycated hemoglobin (HbA1c), fasting glucose, BMI, total cholesterol, and LDL, but had no effect on fasting insulin, HOMA-IR, HDL, triglycerides, or insulin requirements. The reduction in fasting glucose and HbA1c was inversely correlated with body weight. The greatest reduction in fasting blood glucose was seen in the studies of the longest duration.
CONCLUSIONS
Low-GI diets may be useful for glycemic control and may reduce body weight in people with prediabetes or diabetes.
Topics: Blood Glucose; Diabetes Mellitus, Type 1; Diabetes Mellitus, Type 2; Diet; Glycemic Index; Humans; Insulin
PubMed: 31374573
DOI: 10.1093/ajcn/nqz149 -
European Journal of Pharmacology May 2023To update the evidence about the diabetogenic effect of statins. (Meta-Analysis)
Meta-Analysis Review
AIMS
To update the evidence about the diabetogenic effect of statins.
METHODS
We searched for randomized-controlled trials reporting the effects of statin therapy on glycosylated hemoglobin (HbA1c) and/or homeostatic model insulin resistance (i.e., HOMA-IR) as indexes of diabetes. Studies were classified between the ones testing normal vs individuals with already altered glycemic control (HbA1c ≥ 6.5%; and HOMA-IR ≥ 2.15). Furthermore, studies were separated by statin type and dosage prescribed. Data are presented as mean difference (MD) and 95% confidence intervals.
RESULTS
A total of 67 studies were included in the analysis (>25,000 individuals). In individuals with altered glycemic control, statins increased HbA1c levels (MD 0.21%, 95% CI 0.16-to-0.25) and HOMA-IR index (MD 0.31, 95% CI 0.24-to-0.38). In individuals with normal glycemic control, statin increased HbA1c (MD 1.33%, 95% CI 1.31-to-1.35) and HOMA-IR (MD 0.49, 95% CI 0.41-to-0.58) in comparison to the placebo groups. The dose or type of statins did not modulate the diabetogenic effect.
CONCLUSIONS
Statins, slightly but significantly raise indexes of diabetes in individuals with adequate or altered glycemic control. The diabetogenic effect does not seem to be influenced by the type or dosage of statin prescribed.
Topics: Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Glycated Hemoglobin; Insulin Resistance; Glycemic Control; Diabetes Mellitus; Blood Glucose; Insulin; Diabetes Mellitus, Type 2
PubMed: 36965747
DOI: 10.1016/j.ejphar.2023.175672 -
PLoS Medicine Jul 2016Effects of major dietary macronutrients on glucose-insulin homeostasis remain controversial and may vary by the clinical measures examined. We aimed to assess how... (Meta-Analysis)
Meta-Analysis Review
Effects of Saturated Fat, Polyunsaturated Fat, Monounsaturated Fat, and Carbohydrate on Glucose-Insulin Homeostasis: A Systematic Review and Meta-analysis of Randomised Controlled Feeding Trials.
BACKGROUND
Effects of major dietary macronutrients on glucose-insulin homeostasis remain controversial and may vary by the clinical measures examined. We aimed to assess how saturated fat (SFA), monounsaturated fat (MUFA), polyunsaturated fat (PUFA), and carbohydrate affect key metrics of glucose-insulin homeostasis.
METHODS AND FINDINGS
We systematically searched multiple databases (PubMed, EMBASE, OVID, BIOSIS, Web-of-Knowledge, CAB, CINAHL, Cochrane Library, SIGLE, Faculty1000) for randomised controlled feeding trials published by 26 Nov 2015 that tested effects of macronutrient intake on blood glucose, insulin, HbA1c, insulin sensitivity, and insulin secretion in adults aged ≥18 years. We excluded trials with non-isocaloric comparisons and trials providing dietary advice or supplements rather than meals. Studies were reviewed and data extracted independently in duplicate. Among 6,124 abstracts, 102 trials, including 239 diet arms and 4,220 adults, met eligibility requirements. Using multiple-treatment meta-regression, we estimated dose-response effects of isocaloric replacements between SFA, MUFA, PUFA, and carbohydrate, adjusted for protein, trans fat, and dietary fibre. Replacing 5% energy from carbohydrate with SFA had no significant effect on fasting glucose (+0.02 mmol/L, 95% CI = -0.01, +0.04; n trials = 99), but lowered fasting insulin (-1.1 pmol/L; -1.7, -0.5; n = 90). Replacing carbohydrate with MUFA lowered HbA1c (-0.09%; -0.12, -0.05; n = 23), 2 h post-challenge insulin (-20.3 pmol/L; -32.2, -8.4; n = 11), and homeostasis model assessment for insulin resistance (HOMA-IR) (-2.4%; -4.6, -0.3; n = 30). Replacing carbohydrate with PUFA significantly lowered HbA1c (-0.11%; -0.17, -0.05) and fasting insulin (-1.6 pmol/L; -2.8, -0.4). Replacing SFA with PUFA significantly lowered glucose, HbA1c, C-peptide, and HOMA. Based on gold-standard acute insulin response in ten trials, PUFA significantly improved insulin secretion capacity (+0.5 pmol/L/min; 0.2, 0.8) whether replacing carbohydrate, SFA, or even MUFA. No significant effects of any macronutrient replacements were observed for 2 h post-challenge glucose or insulin sensitivity (minimal-model index). Limitations included a small number of trials for some outcomes and potential issues of blinding, compliance, generalisability, heterogeneity due to unmeasured factors, and publication bias.
CONCLUSIONS
This meta-analysis of randomised controlled feeding trials provides evidence that dietary macronutrients have diverse effects on glucose-insulin homeostasis. In comparison to carbohydrate, SFA, or MUFA, most consistent favourable effects were seen with PUFA, which was linked to improved glycaemia, insulin resistance, and insulin secretion capacity.
Topics: Adult; Blood Glucose; Dietary Carbohydrates; Fats, Unsaturated; Fatty Acids, Monounsaturated; Fatty Acids, Unsaturated; Glycated Hemoglobin; Homeostasis; Humans; Insulin; Randomized Controlled Trials as Topic
PubMed: 27434027
DOI: 10.1371/journal.pmed.1002087 -
Ageing Research Reviews Nov 2017This systematic review investigated whether the insulin sensitiser metformin has a geroprotective effect in humans. Pubmed and Embase were searched along with databases... (Meta-Analysis)
Meta-Analysis Review
This systematic review investigated whether the insulin sensitiser metformin has a geroprotective effect in humans. Pubmed and Embase were searched along with databases of unpublished studies. Eligible research investigated the effect of metformin on all-cause mortality or diseases of ageing relative to non-diabetic populations or diabetics receiving other therapies with adjustment for disease control achieved. Overall, 260 full-texts were reviewed and 53 met the inclusion criteria. Diabetics taking metformin had significantly lower all-cause mortality than non-diabetics (hazard ratio (HR)=0.93, 95%CI 0.88-0.99), as did diabetics taking metformin compared to diabetics receiving non-metformin therapies (HR=0.72, 95%CI 0.65-0.80), insulin (HR=0.68, 95%CI 0.63-0.75) or sulphonylurea (HR=0.80, 95%CI 0.66-0.97). Metformin users also had reduced cancer compared to non-diabetics (rate ratio=0.94, 95%CI 0.92-0.97) and cardiovascular disease (CVD) compared to diabetics receiving non-metformin therapies (HR=0.76, 95%CI 0.66-0.87) or insulin (HR=0.78, 95%CI 0.73-0.83). Differences in baseline characteristics were observed which had the potential to bias findings, although statistical adjustments were made. The apparent reductions in all-cause mortality and diseases of ageing associated with metformin use suggest that metformin could be extending life and healthspans by acting as a geroprotective agent.
Topics: Aging; Cardiovascular Diseases; Case-Control Studies; Diabetes Mellitus, Type 2; Humans; Hypoglycemic Agents; Insulin; Metformin; Neoplasms; Observational Studies as Topic; Treatment Outcome
PubMed: 28802803
DOI: 10.1016/j.arr.2017.08.003 -
BMJ Open Aug 2017To summarise incidence and prevalence of diabetic ketoacidosis (DKA) in adults with type 1 diabetes (T1D) for the overall patient population and different subgroups... (Review)
Review
OBJECTIVES
To summarise incidence and prevalence of diabetic ketoacidosis (DKA) in adults with type 1 diabetes (T1D) for the overall patient population and different subgroups (age, sex, geographical region, ethnicity and type of insulin administration).
DESIGN
Systematic literature review (SLR).
DATA SOURCES
Medline (via PubMed) and Embase (1 January 2000 to 23 June 2016).
STUDY SELECTION
Peer-reviewed observational studies with reported data on the incidence or prevalence of DKA in T1D adults were included. A single reviewer completed the study screening and selection process and a second reviewer performed an additional screening of approximately 20% of the publications; two reviewers independently conducted the quality assessment; the results were narratively synthesised.
RESULTS
Out of 1082 articles, 19 met the inclusion and exclusion criteria, with two additional studies identified that did not specify the patient age range and are therefore not included in the SLR. Overall, eight studies reported incidence with a range of 0-56 per 1000 person-years (PYs), with one outlying study reporting an incidence of 263 per 1000 PYs. Eleven studies reported prevalence with a range of 0-128 per 1000 people. Prevalence of DKA decreased with increasing age. Subgroup analyses were performed using data from no more than two studies per subgroup. There was a higher prevalence of DKA reported in women, non-whites and patients treated with insulin injections compared with men, whites and patients using continuous subcutaneous insulin infusion pumps, respectively.
CONCLUSIONS
To our knowledge, this is the first SLR on the epidemiology of DKA in T1D adults. Despite an increasing prevalence of T1D in recent years, DKA in adults has been poorly characterised. In an era when the benefit-risk profiles of new antidiabetic therapies are being evaluated, including the potential risk of DKA, there is a clear need to better elucidate the expected rate of DKA among T1D adults.
Topics: Adult; Diabetes Mellitus, Type 1; Diabetic Ketoacidosis; Female; Humans; Hypoglycemic Agents; Infusion Pumps; Injections; Insulin; Male
PubMed: 28765134
DOI: 10.1136/bmjopen-2017-016587 -
PLoS Medicine Aug 2019Metformin is increasingly offered as an acceptable and economic alternative to insulin for treatment of gestational diabetes mellitus (GDM) in many countries. However,... (Comparative Study)
Comparative Study Meta-Analysis
BACKGROUND
Metformin is increasingly offered as an acceptable and economic alternative to insulin for treatment of gestational diabetes mellitus (GDM) in many countries. However, the impact of maternal metformin treatment on the trajectory of fetal, infant, and childhood growth is unknown.
METHODS AND FINDINGS
PubMed, Ovid Embase, Medline, Web of Science, ClinicalTrials.gov, and the Cochrane database were systematically searched (from database inception to 26 February 2019). Outcomes of GDM-affected pregnancies randomised to treatment with metformin versus insulin were included (randomised controlled trials and prospective randomised controlled studies) from cohorts including European, American, Asian, Australian, and African women. Studies including pregnant women with pre-existing diabetes or non-diabetic women were excluded, as were trials comparing metformin treatment with oral glucose-lowering agents other than insulin. Two reviewers independently assessed articles for eligibility and risk of bias, and conflicts were resolved by a third reviewer. Outcome measures were parameters of fetal, infant, and childhood growth, including weight, height, BMI, and body composition. In total, 28 studies (n = 3,976 participants) met eligibility criteria and were included in the meta-analysis. No studies reported fetal growth parameters; 19 studies (n = 3,723 neonates) reported measures of neonatal growth. Neonates born to metformin-treated mothers had lower birth weights (mean difference -107.7 g, 95% CI -182.3 to -32.7, I2 = 83%, p = 0.005) and lower ponderal indices (mean difference -0.13 kg/m3, 95% CI -0.26 to 0.00, I2 = 0%, p = 0.04) than neonates of insulin-treated mothers. The odds of macrosomia (odds ratio [OR] 0.59, 95% CI 0.46 to 0.77, p < 0.001) and large for gestational age (OR 0.78, 95% CI 0.62 to 0.99, p = 0.04) were lower following maternal treatment with metformin compared to insulin. There was no difference in neonatal height or incidence of small for gestational age between groups. Two studies (n = 411 infants) reported measures of infant growth (18-24 months of age). In contrast to the neonatal phase, metformin-exposed infants were significantly heavier than those in the insulin-exposed group (mean difference 440 g, 95% CI 50 to 830, I2 = 4%, p = 0.03). Three studies (n = 520 children) reported mid-childhood growth parameters (5-9 years). In mid-childhood, BMI was significantly higher (mean difference 0.78 kg/m2, 95% CI 0.23 to 1.33, I2 = 7%, p = 0.005) following metformin exposure than following insulin exposure, although the difference in absolute weights between the groups was not significantly different (p = 0.09). Limited evidence (1 study with data treated as 2 cohorts) suggested that adiposity indices (abdominal [p = 0.02] and visceral [p = 0.03] fat volumes) may be higher in children born to metformin-treated compared to insulin-treated mothers. Study limitations include heterogeneity in metformin dosing, heterogeneity in diagnostic criteria for GDM, and the scarcity of reporting of childhood outcomes.
CONCLUSIONS
Following intrauterine exposure to metformin for treatment of maternal GDM, neonates are significantly smaller than neonates whose mothers were treated with insulin during pregnancy. Despite lower average birth weight, metformin-exposed children appear to experience accelerated postnatal growth, resulting in heavier infants and higher BMI by mid-childhood compared to children whose mothers were treated with insulin. Such patterns of low birth weight and postnatal catch-up growth have been reported to be associated with adverse long-term cardio-metabolic outcomes. This suggests a need for further studies examining longitudinal perinatal and childhood outcomes following intrauterine metformin exposure. This review protocol was registered with PROSPERO under registration number CRD42018117503.
Topics: Child Development; Child, Preschool; Diabetes, Gestational; Female; Humans; Hypoglycemic Agents; Infant; Infant, Newborn; Insulin; Metformin; Pregnancy
PubMed: 31386659
DOI: 10.1371/journal.pmed.1002848 -
Endocrine, Metabolic & Immune Disorders... 2021Type one diabetes mellitus (T1DM) is an autoimmune disease characterized by gradual destruction of beta cells in islets of Langerhans. Teplizumab is a humanized anti-... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Type one diabetes mellitus (T1DM) is an autoimmune disease characterized by gradual destruction of beta cells in islets of Langerhans. Teplizumab is a humanized anti- CD3 monoclonal antibody, which may have beneficial effects for T1DM patients.
OBJECTIVE
The aim of the study was to assess the safety and efficacy of teplizumab in T1DM patients.
METHODS
We searched electronic databases using related keywords for randomized clinical trials assessing the safety and efficacy of teplizumab. We evaluated the retrieved citations for eligibility, and we extracted the data and then analyzed it using Review Manager Software.
RESULTS
We included eight randomized clinical trials with 866 patients. Teplizumab was associated with lower insulin use than placebo at 6 months (MD = -0.17, 95% CI [-0.24, -0.09], P < 0.001), 12 months (MD = -0.12, 95% CI [-0.18, -0.06], P < 0.001), 18 months (MD = -0.22, 95% CI [-0.32, -0.11], P < 0.001) and 24 months (MD = -0.17, 95% CI [-0.28, -0.06], P = 0.003). The area under the curve of C-peptide was significantly increased in teplizumab group at 12 months (MD = 0.08, 95% CI [0.01, 0.15], P = 0.03), 18 months (MD = 0.13, 95% CI [0.01, 0.25], P = 0.03) and 24 months (MD = 0.13, 95% CI [0.01, 0.24], P = 0.03). No significant effect of teplizumab on HbA1c levels was observed at any time point. Teplizumab was found to be associated with some side effects such as lymphopenia, skin and subcutaneous tissue disorders.
CONCLUSION
Teplizumab is associated with lower insulin use and higher AUC of C-peptide in type 1 diabetic patients with no significant effect on Hb1c levels. Besides, teplizumab has shown some adverse effects.
Topics: Antibodies, Monoclonal, Humanized; Diabetes Mellitus, Type 1; Drug-Related Side Effects and Adverse Reactions; Glycated Hemoglobin; Humans; Insulin; Insulin-Secreting Cells; Treatment Outcome
PubMed: 33302842
DOI: 10.2174/1871530320999201209222921 -
Acta Diabetologica May 2023To expand the evidence base for the clinical use of metformin, we conducted a meta-analysis of randomized controlled trials (RCTs) comparing the efficacy and safety of... (Meta-Analysis)
Meta-Analysis Review
Short-term neonatal outcomes in women with gestational diabetes treated using metformin versus insulin: a systematic review and meta-analysis of randomized controlled trials.
AIMS
To expand the evidence base for the clinical use of metformin, we conducted a meta-analysis of randomized controlled trials (RCTs) comparing the efficacy and safety of metformin versus insulin with respect to short-term neonatal outcomes.
METHODS
A comprehensive search of electronic databases (PubMed, Embase, Cochrane Library, and Web of Science) was performed. Two reviewers extracted the data and calculated pooled estimates by use of a random-effects model. In total, 24 studies involving 4355 participants met the eligibility criteria and were included in the quantitative analyses.
RESULTS
Unlike insulin, metformin lowered neonatal birth weights (mean difference - 122.76 g; 95% confidence interval [CI] - 178.31, - 67.21; p < 0.0001), the risk of macrosomia (risk ratio [RR] 0.68; 95% CI 0.54, 0.86; p = 0.001), the incidence of neonatal intensive care unit admission (RR 0.73; 95% CI 0.61, 0.88; p = 0.0009), and the incidence of neonatal hypoglycemia (RR 0.65; 95% CI 0.52, 0.81; p = 0.0001). Subgroup analysis based on the maximum daily oral dose of metformin indicated that metformin-induced neonatal birth weight loss was independent of the oral dose.
CONCLUSIONS
Our meta-analysis provides further evidence that metformin is a safe oral antihyperglycemic drug and has some benefits over insulin when used for the treatment of gestational diabetes, without an increased risk of short-term neonatal adverse outcomes. Metformin may be particularly useful in women with gestational diabetes at high risk for neonatal hypoglycemia, women who want to limit maternal and fetal weight gain, and women with an inability to afford or use insulin safely.
Topics: Pregnancy; Infant, Newborn; Female; Humans; Diabetes, Gestational; Metformin; Insulin; Hypoglycemic Agents; Randomized Controlled Trials as Topic; Hypoglycemia; Birth Weight; Weight Gain
PubMed: 36593391
DOI: 10.1007/s00592-022-02016-5