Methods: A systematic review was done to study the effects of naringin on the metabolic diseases using electronic databases which include Ovid and Scopus using specific descriptors published from the year 2010 till present to provide updated literature on this field. The articles were assessed and chosen based on the criteria in which the mechanisms and effects of naringin on different metabolic diseases were reported.
Results: Thirty-four articles were identified which referred to the studies that correspond to the previously stated criteria. Subsequently after screening for the articles that were published after the year 2010, finally, 19 articles were selected and assessed accordingly. Based on the assessment, naringin could alleviate MetS by reducing visceral obesity, blood glucose, blood pressure, and lipid profile and regulating cytokines.
Conclusions: Naringin is an antioxidant that appears to be efficacious in alleviating MetS by preventing oxidative damage and proinflammatory cytokine release. However, the dosage used in animal studies might not be achieved in human trials. Thus, adequate investigation needs to be conducted to confirm naringin's effects on humans.
OBJECTIVES: To assess the effects of low glycaemic index or low glycaemic load diets on weight loss in people with overweight or obesity.
SEARCH METHODS: We searched CENTRAL, MEDLINE, one other database, and two clinical trials registers from their inception to 25 May 2022. We did not apply any language restrictions.
SELECTION CRITERIA: We included RCTs with a minimum duration of eight weeks comparing low GI/GL diets to higher GI/GL diets or any other diets in people with overweight or obesity.
DATA COLLECTION AND ANALYSIS: We used standard Cochrane methods. We conducted two main comparisons: low GI/GL diets versus higher GI/GL diets and low GI/GL diets versus any other diet. Our main outcomes included change in body weight and body mass index, adverse events, health-related quality of life, and mortality. We used GRADE to assess the certainty of the evidence for each outcome.
MAIN RESULTS: In this updated review, we included 10 studies (1210 participants); nine were newly-identified studies. We included only one study from the previous version of this review, following a revision of inclusion criteria. We listed five studies as 'awaiting classification' and one study as 'ongoing'. Of the 10 included studies, seven compared low GI/GL diets (233 participants) with higher GI/GL diets (222 participants) and three studies compared low GI/GL diets (379 participants) with any other diet (376 participants). One study included children (50 participants); one study included adults aged over 65 years (24 participants); the remaining studies included adults (1136 participants). The duration of the interventions varied from eight weeks to 18 months. All trials had an unclear or high risk of bias across several domains. Low GI/GL diets versus higher GI/GL diets Low GI/GL diets probably result in little to no difference in change in body weight compared to higher GI/GL diets (mean difference (MD) -0.82 kg, 95% confidence interval (CI) -1.92 to 0.28; I2 = 52%; 7 studies, 403 participants; moderate-certainty evidence). Evidence from four studies reporting change in body mass index (BMI) indicated low GI/GL diets may result in little to no difference in change in BMI compared to higher GI/GL diets (MD -0.45 kg/m2, 95% CI -1.02 to 0.12; I2 = 22%; 186 participants; low-certainty evidence)at the end of the study periods. One study assessing participants' mood indicated that low GI/GL diets may improve mood compared to higher GI/GL diets, but the evidence is very uncertain (MD -3.5, 95% CI -9.33 to 2.33; 42 participants; very low-certainty evidence). Two studies assessing adverse events did not report any adverse events; we judged this outcome to have very low-certainty evidence. No studies reported on all-cause mortality. For the secondary outcomes, low GI/GL diets may result in little to no difference in fat mass compared to higher GI/GL diets (MD -0.86 kg, 95% CI -1.52 to -0.20; I2 = 6%; 6 studies, 295 participants; low certainty-evidence). Similarly, low GI/GL diets may result in little to no difference in fasting blood glucose level compared to higher GI/GL diets (MD 0.12 mmol/L, 95% CI 0.03 to 0.21; I2 = 0%; 6 studies, 344 participants; low-certainty evidence). Low GI/GL diets versus any other diet Low GI/GL diets probably result in little to no difference in change in body weight compared to other diets (MD -1.24 kg, 95% CI -2.82 to 0.34; I2 = 70%; 3 studies, 723 participants; moderate-certainty evidence). The evidence suggests that low GI/GL diets probably result in little to no difference in change in BMI compared to other diets (MD -0.30 kg in favour of low GI/GL diets, 95% CI -0.59 to -0.01; I2 = 0%; 2 studies, 650 participants; moderate-certainty evidence). Two adverse events were reported in one study: one was not related to the intervention, and the other, an eating disorder, may have been related to the intervention. Another study reported 11 adverse events, including hypoglycaemia following an oral glucose tolerance test. The same study reported seven serious adverse events, including kidney stones and diverticulitis. We judged this outcome to have low-certainty evidence. No studies reported on health-related quality of life or all-cause mortality. For the secondary outcomes, none of the studies reported on fat mass. Low GI/GL diets probably do not reduce fasting blood glucose level compared to other diets (MD 0.03 mmol/L, 95% CI -0.05 to 0.12; I2 = 0%; 3 studies, 732 participants; moderate-certainty evidence). AUTHORS' CONCLUSIONS: The current evidence indicates there may be little to no difference for all main outcomes between low GI/GL diets versus higher GI/GL diets or any other diet. There is insufficient information to draw firm conclusions about the effect of low GI/GL diets on people with overweight or obesity. Most studies had a small sample size, with only a few participants in each comparison group. We rated the certainty of the evidence as moderate to very low. More well-designed and adequately-powered studies are needed. They should follow a standardised intervention protocol, adopt objective outcome measurement since blinding may be difficult to achieve, and make efforts to minimise loss to follow-up. Furthermore, studies in people from a wide range of ethnicities and with a wide range of dietary habits, as well as studies in low- and middle-income countries, are needed.
AIM: To investigate the effects of food order on postprandial glucose (PPG) excursion, in Indian adults with normal (NL) and overweight/obese (OW) Body Mass Index.
METHODS: This randomised crossover study was conducted at a Malaysian university among Indian adults without diabetes. The participants consumed isocaloric test meals at three study visits based on randomised food orders: carbohydrate first/protein last (CF); protein first/carbohydrate last (CL); and a composite meal containing carbohydrate and protein (CM). Capillary blood glucose was measured at baseline, 30, 60, 90 and 120 minutes after starting the meal.
RESULTS: The CL food order had a blunting effect on PPG excursion at 30 and 60 minutes (p < 0.01). The CL food order resulted in lower glucose peak when compared with the CF and CM food order (p < 0.001). The CL food order resulted in lower incremental glucose peak (mmol/L) (NL: CF 3.9 ± 0.3, CM 3.0 ± 0.3, CL 2.0 ± 0.2; OW: CF 2.9 ± 0.3, CM 2.5 ± 0.3, CL 1.8 ± 0.2) and iAUC 0-120 min (mmol/Lxmin) (NL: CF 272.4 ± 26.7, CM 206.2 ± 30.3, CL 122.0 ± 14.8; OW: CF 193.2 ± 23.1, CM 160.1 ± 21.7, CL 113.6 ± 15.3) when compared with the CF food order (p < 0.001). The effect of food order on postprandial excursion did not differ between the NL (n = 14) and the OW (n = 17) groups.
CONCLUSION: In participants with normal and overweight/obese BMI, consuming food in the protein first/carbohydrate last order had the biggest effect in reducing PPG excursion.
AIM: This study aimed to compare the efficacy of adding Insulin to dual OHAs (Sitagliptin + Metformin) against adding a third OHA to Sitagliptin + Metformin in achieving glycemic control among patients with uncontrolled T2DM.
METHOD: A pre-post study was conducted between 21 September 2023 and 21 December 2023 at Services Hospital Peshawar, Pakistan. Patients with uncontrolled T2DM with >7% HbA1c were divided into group 1 (Sitagliptin + Metformin plus a third OHA), and group 2 (Sitagliptin + Metformin plus pre-mixed Insulin 70/30). Glycemic control based on HbA1c values, fasting and random blood sugar levels, lipid profile, and body weight were evaluated after 3 months of therapy. The pre- and post- effect was compared by using a paired t-test.
RESULTS: The study included n = 80 patients with T2DM. Between groups 1 and 2, no significant difference was found in HbA1c values (9.1 vs. 9, with p = 0.724). However, BMI, cholesterol, and LDL significantly decreased in group 1 compared to group 2 (p<0.001 vs. p = 0.131, p = 0.023 vs. p = 0.896, and p = 0.003 vs. p = 0.395, respectively). Additionally, the incidence of hypoglycemic episodes was significantly lower in group 1 (7.5%) than in group 2 (47.5%, p = 0.004). No significant difference was observed between the triple OHA and dual OHA plus Insulin regimens in achieving glycemic control.
CONCLUSION: The triple OHA regimen improved BMI, cholesterol, and LDL levels, and reduced hypoglycemic episodes more effectively than dual OHA plus Insulin, despite similar HbA1c outcomes, suggesting it may be preferable for uncontrolled T2DM.
METHODS: This study included people living with HIV enrolled in a longitudinal cohort study from 2003 to 2019, receiving antiretroviral therapy (ART), and without prior tuberculosis. BMI at ART initiation was categorized using Asian BMI classifications: underweight (<18.5 kg/m2 ), normal (18.5-22.9 kg/m2 ), overweight (23-24.9 kg/m2 ), and obese (≥25 kg/m2 ). High FBG was defined as a single post-ART FBG measurement ≥126 mg/dL. Factors associated with high FBG were analyzed using Cox regression models stratified by site.
RESULTS: A total of 3939 people living with HIV (63% male) were included. In total, 50% had a BMI in the normal weight range, 23% were underweight, 13% were overweight, and 14% were obese. Median age at ART initiation was 34 years (interquartile range 29-41). Overall, 8% had a high FBG, with an incidence rate of 1.14 per 100 person-years. Factors associated with an increased hazard of high FBG included being obese (≥25 kg/m2 ) compared with normal weight (hazard ratio [HR] = 1.79; 95% confidence interval [CI] 1.31-2.44; p 25 kg/m2 were at increased risk of high FBG. This indicates that regular assessments should be performed in those with high BMI, irrespective of the classification used.
METHODS: A total of 174 subjects were divided into NGT (n=58), pre-DM (n=54), and T2DM (n=62). Plasma total GLP-1 concentrations were measured at 0, 30, and 120 min during a 75-g OGTT. Homeostasis model assessment of insulin resistance (HOMA-IR), HOMA of insulin sensitivity (HOMA-IS), and triglyceride-glucose index (TyG) were calculated.
RESULTS: Total GLP-1 levels at fasting and 30 min were significantly higher in T2DM compared with pre-DM and NGT (27.18 ± 11.56 pmol/L vs. 21.99 ± 10.16 pmol/L vs. 16.24 ± 7.79 pmol/L, p=0.001; and 50.22 ± 18.03 pmol/L vs. 41.05 ± 17.68 pmol/L vs. 31.44 ± 22.59 pmol/L, p<0.001; respectively). Ethnicity was a significant determinant of AUCGLP-1, with the Indians exhibiting higher GLP-1 responses than Chinese and Malays. Indians were the most insulin resistant, whereas Chinese were the most insulin sensitive. The GLP-1 levels were positively correlated with HOMA-IR and TyG but negatively correlated with HOMA-IS. This relationship was evident among Indians who exhibited augmented GLP-1 responses proportionately to their high insulin-resistant states.
CONCLUSION: This is the first study that showed GLP-1 responses are augmented as IR states increase. Fasting and post-OGTT GLP-1 levels are raised in T2DM and pre-DM compared to that in NGT. This raises a possibility of an adaptive compensatory response that has not been reported before. Among the three ethnic groups, the Indians has the highest IR and GLP-1 levels supporting the notion of an adaptive compensatory secretion of GLP-1.