Aquaporins and Adipose Tissue: Lesson from Discovery to Physiopathology and to the Clinic of Aquaporin Adipose (AQP7)

Kishida, Ken

doi:10.1002/9783527629527.ch8

Cited by 1 publication

(1 citation statement)

References 49 publications

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“…Disruption of aquaporin7 causes disturbance of the normal rise of circulating glycerol in human [10] and profound hypoglycemia during prolonged fasting in aquaporin7-deficient mice because of impaired glycerol supply to the liver [11]. Consistently, aquaporin7 is overexpressed in visceral fat accumulation, accompanied by portal hyperglycerolemia and systemic hyperglycemia [12][13][14] (Fig. 1).…”

Section: Characteristics Of Visceral Fatmentioning

confidence: 59%

Molecular Mechanisms of Diabetes and Atherosclerosis: Role of Adiponectin

Kishida

Funahashi²,

Shimomura³

2012

EMIDDT

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Type 2 diabetes mellitus (T2DM) is a disease characterized by inadequate beta-cell response due to progressive insulin resistance that typically accompanies physical inactivity and weight gain. T2DM is associated with substantial morbidity and mortality related to the associated atherosclerotic cardiovascular risks and diabetic vasculopathies, including microangiopathies (e.g., blindness and renal failure) and macroangiopathies (atherosclerosis). The increasing global prevalence of T2DM is linked to the rising rates of obesity, especially abdominal obesity. Visceral fat accumulation is upstream of obesity-related disorders including atherosclerotic cardiovascular disease (ACVD), and is associated with impaired insulin sensitivity and atherosclerosis through dysregulated production of adipocytokines, especially hypoadiponectinemia. This review article discusses the pathophysiological mechanisms responsible for T2DM and atherosclerosis, focusing on adiponectin. Clinical and experimental studies have shown that hypoadiponectinemia contributes to a variety of life style-related diseases including T2DM and atherosclerosis. It is likely that life-style modification, visceral fat reduction and use of medications that increase serum adiponectin levels (e.g., rimonabant, thiazolidinediones, fibrates, angiotensin receptor blocker and mineralocorticoid receptor blockade) when provided in combination can improve hypoadiponectinemia and thus prevent the development of life style-related diseases including T2DM and ACVD.

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