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Association of Gut Intestinal Integrity and Inflammation with Insulin Resistance in Adults Living with HIV in Uganda.
Reid, MJA, Ma, Y, Golovaty, I, Okello, S, Sentongo, R, Feng, M, Tsai, AC, Kakuhikire, B, Tracy, R, Hunt, PW, et al
AIDS patient care and STDs. 2019;(7):299-307
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Abstract
We conducted a cross-sectional study of 148 HIV+ on HIV antiretroviral therapy and 149 HIV- adults in Mbarara, Uganda, to estimate the association between HIV infection and homeostasis model assessment of insulin resistance (HOMA-IR) using multivariable regression analysis. In addition, we evaluated whether intestinal fatty acid-binding protein (I-FABP), monocyte activation markers soluble (s)CD14 and sCD163, and proinflammatory cytokine interleukin 6 (IL-6) mediated this association. HOMA-IR was greater among HIV+ than HIV- adults [median (interquartile range): 1.3 (0.7-2.5) vs. 0.9 (0.5-2.4); pā=ā0.008]. In models adjusted for sociodemographic variables, diet, hypertension, and smoking history, HIV infection was associated with 37% [95% confidence intervals (95% CIs): 5-77] greater HOMA-IR compared with HIV- participants. The magnitude of association was greater when I-FABP was included as a covariate although the additive effect was modest (40% CI: 8-82). By contrast adding sCD14 to the model was associated with greater HOMA-IR (59%; 95% CI: 21-109) among HIV+ participants compared with HIV- participants. Among HIV+ participants, greater CD4 nadir was non-significantly associated with greater HOMA-IR (22%; 95% CI: -2 to 52). Each 5-unit increase in body mass index (BMI; 49% greater HOMA-IR; 95% CI: 18-87) and female sex (71%; 95% CI: 17-150) remained associated in adjusted models. In this study of mainly normal-weight Ugandan adults, HIV infection, female sex, and greater BMI were all associated with greater insulin resistance (IR). This association was strengthened modestly after adjustment for sCD14, suggesting possible distinct immune pathways to IR that are independent of HIV or related to inflammatory changes occurring on HIV treatment.
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Diets high in carbohydrate may not be appropriate for rs328 G carriers with the metabolic syndrome.
Zhang, S, Ma, Y, Guo, H, Wan, W, Xue, K
Asia Pacific journal of clinical nutrition. 2015;(3):546-54
Abstract
The objective of this study was to test how the genetic polymorphisms located within the lipoprotein lipase (LPL) locus would modulate the relationship between a diet high in carbohydrate and insulin resistance related traits in metabolic syndrome adults. A one year nutritional intervention study focusing on education to increase dietary intake of whole grain, vegetable and fruit, and to reduce the intake of sodium, simple sugar and dietary fat (especially cooking oil and pork lard) was conducted. Two districts in Shanghai, China were randomly selected to be the intervention and control group, and patients (n=235) with metabolic syndrome within these two districts were selected based on a multistage sampling method. Fasting glucose was reduced in rs328 CC homozygotes (p=0.028) but not G carriers (p=0.686) within the intervention group. Also an ancillary study with greater statistical power by combining the baseline measurements across both the intervention and control groups was conducted to test the cross-sectional statistical interactions between carbohydrate/fat and lipoprotein lipase genotypes for homeostasis model assessment of insulin resistance/insulin/fasting glucose. Increased carbohydrate intakes were positively associated with homeostasis model assessment of insulin resistance and insulin in rs328 G carriers but not CC homozygotes (p for interaction was 0.025). These results indicate that diet high in carbohydrate may not be suitable for metabolic syndrome rs328 G carriers, calling for the development of personalized dietary intervention for metabolic syndrome subjects.
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Chromium effects on glucose tolerance and insulin sensitivity in persons at risk for diabetes mellitus.
Ali, A, Ma, Y, Reynolds, J, Wise, JP, Inzucchi, SE, Katz, DL
Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists. 2011;(1):16-25
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Abstract
OBJECTIVE To investigate the effects of daily chromium picolinate supplementation on serum measures of glucose tolerance and insulin sensitivity in patients at high risk for type 2 diabetes mellitus. METHODS We conducted a randomized, double-blind, placebo-controlled, modified cross-over clinical trial with 6-month sequences of intervention and placebo followed by a 6-month postintervention assessment. Adult patients with impaired fasting glucose, impaired glucose tolerance, or metabolic syndrome were enrolled. Participants received 6-month sequences of chromium picolinate or placebo at 1 of 2 dosages (500 or 1000 mcg daily). Primary outcome measures were change in fasting plasma glucose, 2-hour plasma glucose during oral glucose tolerance testing, fasting and 2-hour insulin, and homeostasis model assessment of insulin resistance (HOMA-IR). Secondary outcomes included anthropometric measures, blood pressure, endothelial function, hemoglobin A1c, lipids, and urinary microalbumin. RESULTS Fifty-nine participants were enrolled. No changes were seen in glucose level, insulin level, or HOMA-IR (all P>.05) after 6 months of chromium at either dosage level (500 mcg or 1000 mcg daily) when compared with placebo. None of the secondary outcomes improved with either chromium dosage compared with placebo (P>.05). CONCLUSIONS Chromium supplementation does not appear to ameliorate insulin resistance or impaired glucose metabolism in patients at risk for type 2 diabetes and thus is unlikely to attenuate diabetes risk.