Nutritional approaches for managing obesity-associated metabolic diseases

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   Figure 1

   Obesity, inflammation and metabolic dysregulation. During obesity, nutrient overload initiates or exacerbates inflammation in the intestine, adipose tissue and liver. Inflammation, in turn, impairs functions of the liver, adipose tissue, and skeletal muscle to critically contribute to the development of insulin resistance and metabolic dysregulation via working with or without excessive free fatty acids (in particular saturated fatty acids). The interactions between nutrients and host cells e.g., intestinal cells and adipocytes, also generate factors that exert profound actions the brain to alter feeding behaviors, the dysregulation of which contributes significantly to positive energy balance (not depicted). IEC, intestine epithelial cells; IEL, intestine epithelial lymphocytes; DC, dendritic cells; FFA, free fatty acids, and M1/M2, macrophage (MФ) polarization.
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   Figure 2

   Nutritional approaches for managing obesity-associated metabolic impairments in the liver. AMPK, AMP-activated protein kinase; GLUT2, glucose transporter 2; IKK, Iκβ kinases; IR, insulin receptor; IRS1/2, insulin receptor substrate 1/2; JNK, c Jun N-terminal kinase; KC, Kupffer cell; n-3 PUFA, omega-3 polyunsaturated fatty acid; NFκβ, nuclear factor kappa beta; M1, proinflammatory macrophage; M2, anti-inflammatory macrophage; PDK, phosphoinositide-dependent kinase; PI3K, phosphoinositide 3-kinase; pPARα, peroxisome proliferator-activated receptor alpha; ROS, reactive oxygen species; SOD, superoxide dismutase; TG, triglyceride; TGFβ, transforming growth factor beta; TNFα, tumor necrosis factor alpha; Vit D, vitain D; Vit E, vitamin E.
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   Figure 3

   Nutritional approaches for managing obesity-associated metabolic impairments in the small intestine. AMPK, AMP-activated protein kinase; FFAs, free fatty acids; GLUT4, glucose transporter 4; IKK, Iκβ kinases; IR, insulin receptor; IRS1/2, insulin receptor substrate 1/2; JNK, c Jun N-terminal kinase; M1, proinflammatory macrophage; M2, anti-inflammatory macrophage; MCP-1, monocyte chemoattractant protein 1; n-3 PUFA, omega-3 polyunsaturated fatty acid; NFκβ, nuclear factor kappa beta; PDK, phosphoinositide-dependent kinase; PI3K, phosphoinositide 3-kinase; pPARα, peroxisome proliferator-activated receptor alpha; ROS, reactive oxygen species; SIRT1, sirtuin 1; SOD, superoxide dismutase; TG, triglyceride; TGFβ, transforming growth factor beta; TNFα, tumor necrosis factor alpha.
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   Figure 4

   Summary of nutritional approaches for managing obesity-associated metabolic dysregulation. Most of the currently used approaches are shown to be effective at suppressing inflammation, improving insulin sensitivity, and/or decreasing fat deposition. At the integrative level, the combined effects on key metabolic tissues including the intestine, the liver, adipose tissue and muscle bring about improvement of metabolic dysregulation. In addition, nutritional approaches should be combined with healthy life style, e.g., sufficient physical activity and appropriaste circadian clock rhythms of daily life, to maximize the beneficial effects (not depicted). n-3 PUFA, omega-3 polyunsaturated fatty acid; Vit D, vitamin D; Vit E, vitamin E.
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   Figure 5

   Nutritional approaches for managing obesity-associated metabolic impairments in adipose tissue. AMPK, AMP-activated protein kinase; FFAs, free fatty acids; GLUT4, glucose transporter 4; IKK, IIκβ kinases; IR, insulin receptor; IRS1/2, insulin receptor substrate 1/2; JNK, c Jun N-terminal kinase; M1, proinflammatory macrophage; M2, anti-inflammatory macrophage; MCP-1, monocyte chemoattractant protein 1; n-3 PUFA, omega-3 polyunsaturated fatty acid; NFκβ, nuclear factor kappa beta; PDK, phosphoinositide-dependent kinase; PI3K, phosphoinositide 3-kinase; pPARα, peroxisome proliferator-activated receptor alpha; ROS, reactive oxygen species; SIRT1, sirtuin 1; SOD, superoxide dismutase; TG, triglyceride; TGFα, transforming growth factor beta; TNFα, tumor necrosis factor alpha.

• © 2017 Society for Endocrinology