How Obesity Causes Diabetes: Not a Tall Tale

By Mitchell A. Lazar. Science, 2005

649 citations recorded by the source corpus.

Subfields: Endocrine and Autonomic Systems, Epidemiology, Physiology

View Paper: https://www.semanticscholar.org/paper/7b6954e63235748f3c58a64b777016e5d72baeb2

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In Endocrine and Autonomic Systems

In Epidemiology

In Physiology

Citations in the corpus

Interleukin-6 enhances insulin secretion by increasing glucagon-like peptide-1 secretion from L cells and alpha cells (2011, neutral): “Under these conditions, IL-6 is thought to contribute to the induction of insulin resistance and the deterioration of glucose homeostasi”
Interleukin-6 Increases Insulin-Stimulated Glucose Disposal in Humans and Glucose Uptake and Fatty Acid Oxidation In Vitro via AMP-Activated Protein Kinase (2006, background): “It is generally thought that IL-6 promotes insulin resistance (3).”
Nicotinamide mononucleotide, a key NAD+ intermediate, treats the pathophysiology of diet- and age-induced diabetes in mice (2011, background): “Recent studies have raised an interesting possibility that various physiological mechanisms that mediate metabolic adaptation have evolved in response to nutritionally scarce conditions such as famine and drought (Lazar, 2005).”
Adipose tissue as an endocrine organ. (2010, background): “Interleukin-6 (IL-6) Plasma IL-6 levels are increased in type 2 diabetes and are ositively correlated with body mass and plasma free fatty acid conentrations (Lazar, 2005).”
Low-grade inflammation, diet composition and health: current research evidence and its translation (2015, neutral): “Whether, in humans, the placenta alone is responsible is not clear, and it is quite likely that adipose tissue itself, which becomes infiltrated with macrophages, will produce increased amounts of pro-inflammatory cytokines((114)).”
Hypoxia is a potential risk factor for chronic inflammation and adiponectin reduction in adipose tissue of ob/ob and dietary obese mice. (2007, background): “IN OBESITY, chronic inflammation and reduced adiponectin in the white adipose tissue (WAT) contribute to pathogenesis of insulin resistance, which links obesity to many complications, such as type 2 diabetes and cardiovascular diseases (23, 24, 30).”
Environmental obesogens: organotins and endocrine disruption via nuclear receptor signaling. (2006, background): “In calorie-rich modern diets, such thrifty genes may instead lead to obesity and contribute to metabolic syndrome diseases (13, 53).”
Technology, transport, globalization and the nutrition transition food policy (2006, positive): “For instance, these changes are so rapid that many predict countries like China will see a marked increase in total adult mortality rates over the next several decades (Dong et al., 2005; Lazar, 2005; Pan, 2005).”
Hypoxia and adipose tissue function and dysfunction in obesity. (2013, background): “Similarly, the increase in the synthesis and release of IL-6 may contribute to resistance, given the link between this cytokine and insulin sensitivity (107, 108, 170).”
TOR signaling in growth and metabolism. (2006, background): “PPARγ plays a critical role in adipogenesis and lipid accumulation and is therefore referred to as one of the so-called “thrifty genes” that are responsible for efficient storage of energy (Lazar, 2005 and references therein).”
EDC-2: The Endocrine Society's Second Scientific Statement on Endocrine-Disrupting Chemicals. (2015, background): “adipocytes or are not taken up by adipocytes (265, 266).”