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Inflammatory 12/15-lipoxygenase products impair insulin signaling

  1. Top of page
  2. Inflammatory 12/15-lipoxygenase products impair insulin signaling
  3. High glycemic index diet quickly lowers plasma antioxidant levels
  4. Pramlintide/metreleptin: a two-pronged approach to weight loss
  5. Weight loss reverses pattern B lipoprotein phenotype

Inflammation is associated with visceral obesity. The 12/15-lipoxygenase (12/15-LO) enzyme is posited to induce inflammatory changes in blood vessels that promote the development of atherosclerosis and type 2 diabetes. However, the enzyme's direct effect on adipocytes has not been assessed. Evaluating the effect of the leukocyte-12/15-LO on 3T3-L1 adipocytes, Chakrabarti and colleagues provide a report on the localized proinflammatory influence of this lipoxygenase product. Murine adipocytes treated with 12/15-LO leukocytes showed cytokine upregulation, including elevated tumor necrosis factor-a, interleukin-6 and monocyte chemoattractant protein 1 expression, adiponectin downregulation, and impaired insulin signaling. The findings support the role of 12/15-LO in establishing the inflammation and insulin resistance characteristics of obesity. See page 1657

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High glycemic index diet quickly lowers plasma antioxidant levels

  1. Top of page
  2. Inflammatory 12/15-lipoxygenase products impair insulin signaling
  3. High glycemic index diet quickly lowers plasma antioxidant levels
  4. Pramlintide/metreleptin: a two-pronged approach to weight loss
  5. Weight loss reverses pattern B lipoprotein phenotype

High postprandial blood glucose levels, which may result from consuming a diet rich in foods with a high glycemic index (GI), can contribute to cardiovascular disease and diabetes. Given that hyperglycemia promotes the excess production of superoxide anions, oxidative stress may be the first step in a cascade of events induced by a high-GI diet. In a new crossover feeding study of overweight individuals, Botero and colleagues found that a high-GI diet significantly reduces the total antioxidant capacity of blood plasma after just one week, when compared with a low-GI diet. The findings suggest that reduced total antioxidant capacity may serve as an early event in the metabolic changes that link dietary GI to cardiometabolic disease. See page 1664

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Pramlintide/metreleptin: a two-pronged approach to weight loss

  1. Top of page
  2. Inflammatory 12/15-lipoxygenase products impair insulin signaling
  3. High glycemic index diet quickly lowers plasma antioxidant levels
  4. Pramlintide/metreleptin: a two-pronged approach to weight loss
  5. Weight loss reverses pattern B lipoprotein phenotype

Energy homeostasis depends on the complex interaction between long-term adiposity signals, such as leptin, and short-term satiety signals. Agonists targeting only one of these arms of control have demonstrated limited success in achieving meaningful weight loss. A translational research study conducted by Ravussin et al. assessed the efficacy of a combinatorial drug regimen that targets both sides of this feedback system. Patients who received the amylin agonist metreleptin together with the leptin agonist pramlintide showed a weight loss of nearly 13%, as compared with the 8% loss attained by patients treated with either metreleptin or pramlintide alone. This first clinical trial of a combinatorial neurohormonal treatment provides initial evidence for the joint effectiveness of these therapies in inducing significant weight loss. See page 1736.

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Weight loss reverses pattern B lipoprotein phenotype

  1. Top of page
  2. Inflammatory 12/15-lipoxygenase products impair insulin signaling
  3. High glycemic index diet quickly lowers plasma antioxidant levels
  4. Pramlintide/metreleptin: a two-pronged approach to weight loss
  5. Weight loss reverses pattern B lipoprotein phenotype

Overweight and a diet high in carbohydrates are thought to contribute to an atherogenic lipoprotein phenotype characterized by elevated triglyceride levels, reduced high-density lipoprotein cholesterol, and an increased concentration of small, dense low-density lipoprotein cholesterol (LDL) particles known as the pattern B LDL subclass. New research shows that this LDL phenotype and its related lipid abnormalities can undergo conversion to pattern A through a reduced-calorie weight-loss regimen. Fifty-eight percent of men with the pattern B profile at baseline who lost weight reverted to a pattern A phenotype, with 81% of patients who reached a normal-range BMI achieving conversion. Despite evidence of a genetic component to atherogenic dyslipidemia, this reduction of small, dense LDL particles indicates that weight loss and adiposity normalization may help reverse an atherogenic lipoprotein phenotype. See page 1768

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