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Al-Hussaini, H.

Publications and source records attributed to Al-Hussaini, H..

2 recordsLinked to original sources

The Hidden Cost of Blue Light: Multiorgan Pathology Induced by LED Exposure in Mice

Life evolved under broad-spectrum sunlight (300-3500 nm), but most modern light-emitting diodes (LEDs) emit within a restricted visible range (350-650 nm) leaving lighting environments that are short-wavelength dominant. We ask if chronic 450nm exposure dominant in LEDs alters metabolism and organ integrity in ageing mice environmentally exposed at 13 mW/cm{superscript 2} for 5 h/day over 40 weeks, at an intensity within the range of human environmental exposures. Mice exhibited progressive weight gain despite reduced food intake, with altered glucose tolerance and insulin sensitivity over time. White adipose tissue mass increased, while brown adipose tissue weight and UCP1 protein levels remained unchanged. Relative organ weights (heart, liver, kidney, testis) were each reduced by ~10%, with histopathology revealing fat deposition, hepatocellular degeneration, renal tubular damage, steatosis, and impaired testicular architecture. These findings demonstrate that chronic 450 nm light exposure is associated with metabolic alterations and multiorgan pathology in mice.

pathology↗

Glucose intolerance induces anxiety-like behaviors independent of obesity and insulin resistance in a novel model of nutritional metabolic stress

Type 2 diabetes (T2D) and its comorbidities are a major public health concern. In addition to peripheral tissues, T2D also impacts the central nervous system leading to neurocognitive impairments, including memory deficits, anxiety, and depression. The metabolic determinants of these neurocognitive impairments remain unidentified. Here, we used a novel proprietary high-fat diet, in which glucose intolerance precedes weight gain, to decipher the metabolic determinants of neurocognitive affects. We show that this model exhibits anxiety-like behaviors, without eliciting depression nor recognition memory deficits. Long-term feeding leads to weight gain, brain glucose hypometabolism and impaired recognition memory alongside the early onset anxiety-like behavior. Using an established genetic model of T2D (db/db) and of diet-induced obesity we show that additional insulin resistance and obesity are associated with depressive-like behaviors and recognition memory deficits. Our findings indicate that glucose intolerance alone can elicit anxiety-like behaviors. Through this study we also provide a novel nutritional model to characterize the discrete effects of glucose intolerance on cognition, behavior, and the physiology of metabolic disease.

animal behavior and cognition↗