Immunology and Microbiology Department, Dasman Diabetes Institute, Kuwait City, Kuwait.
Animal and Imaging Core Facility, Dasman Diabetes Institute, Kuwait City, Kuwait.
Front Public Health. 2023 Mar 16;11:1115333. doi: 10.3389/fpubh.2023.1115333. eCollection 2023.
Both obesity and a poor diet are considered major risk factors for triggering insulin resistance syndrome (IRS) and the development of type 2 diabetes mellitus (T2DM). Owing to the impact of low-carbohydrate diets, such as the keto diet and the Atkins diet, on weight loss in individuals with obesity, these diets have become an effective strategy for a healthy lifestyle. However, the impact of the ketogenic diet on IRS in healthy individuals of a normal weight has been less well researched. This study presents a cross-sectional observational study that aimed to investigate the effect of low carbohydrate intake in healthy individuals of a normal weight with regard to glucose homeostasis, inflammatory, and metabolic parameters.
The study included 120 participants who were healthy, had a normal weight (BMI 25 kg/m), and had no history of a major medical condition. Self-reported dietary intake and objective physical activity measured by accelerometry were tracked for 7 days. The participants were divided into three groups according to their dietary intake of carbohydrates: the low-carbohydrate (LC) group (those consuming <45% of their daily energy intake from carbohydrates), the recommended range of carbohydrate (RC) group (those consuming 45-65% of their daily energy intake from carbohydrates), and the high-carbohydrate (HC) group (those consuming more than 65% of their daily energy intake from carbohydrates). Blood samples were collected for the analysis of metabolic markers. HOMA of insulin resistance (HOMA-IR) and HOMA of β-cell function (HOMA-β), as well as C-peptide levels, were used for the evaluation of glucose homeostasis.
Low carbohydrate intake (<45% of total energy) was found to significantly correlate with dysregulated glucose homeostasis as measured by elevations in HOMA-IR, HOMA-β% assessment, and C-peptide levels. Low carbohydrate intake was also found to be coupled with lower serum bicarbonate and serum albumin levels, with an increased anion gap indicating metabolic acidosis. The elevation in C-peptide under low carbohydrate intake was found to be positively correlated with the secretion of IRS-related inflammatory markers, including FGF2, IP-10, IL-6, IL-17A, and MDC, but negatively correlated with IL-3.
Overall, the findings of the study showed that, for the first time, low-carbohydrate intake in healthy individuals of a normal weight might lead to dysfunctional glucose homeostasis, increased metabolic acidosis, and the possibility of triggering inflammation by C-peptide elevation in plasma.
肥胖和不良饮食都被认为是引发胰岛素抵抗综合征(IRS)和 2 型糖尿病(T2DM)的主要危险因素。由于低碳水化合物饮食(如生酮饮食和阿特金斯饮食)对肥胖个体的体重减轻的影响,这些饮食已成为健康生活方式的有效策略。然而,生酮饮食对正常体重健康个体 IRS 的影响研究较少。本研究提出了一项横断面观察性研究,旨在调查正常体重健康个体中低碳水化合物摄入对葡萄糖稳态、炎症和代谢参数的影响。
该研究纳入了 120 名健康、体重正常(BMI 25kg/m²)且无重大疾病史的参与者。通过加速度计跟踪 7 天的自我报告饮食摄入和客观体力活动。参与者根据碳水化合物的饮食摄入量分为三组:低碳水化合物(LC)组(每日能量摄入中碳水化合物<45%)、推荐范围的碳水化合物(RC)组(每日能量摄入中碳水化合物 45-65%)和高碳水化合物(HC)组(每日能量摄入中碳水化合物>65%)。采集血样进行代谢标志物分析。使用 HOMA 胰岛素抵抗指数(HOMA-IR)和 HOMA-β 细胞功能指数(HOMA-β)以及 C 肽水平评估葡萄糖稳态。
研究发现,低碳水化合物摄入(<45%总能量)与 HOMA-IR 升高、HOMA-β%评估和 C 肽水平升高所衡量的葡萄糖稳态失调显著相关。低碳水化合物摄入还与血清碳酸氢盐和血清白蛋白水平降低相关,阴离子间隙增加表明代谢性酸中毒。C 肽在低碳水化合物摄入下的升高与 IRS 相关炎症标志物的分泌呈正相关,包括 FGF2、IP-10、IL-6、IL-17A 和 MDC,但与 IL-3 呈负相关。
总的来说,该研究首次表明,正常体重健康个体的低碳水化合物摄入可能导致葡萄糖稳态功能障碍、代谢性酸中毒增加,以及 C 肽在血浆中升高引发炎症的可能性。