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Ritz, D.

Publications and source records attributed to Ritz, D..

2 recordsLinked to original sources

Abiotic drivers of protein abundance variation among natural populations

Identifying when and where environmental change induces molecular responses in natural populations is an important goal in contemporary ecology. It can aid in identifying molecular signatures of populations experiencing stressful conditions and potentially inform if species are approaching the limits of their tolerance niches. Achieving this goal is hampered by our limited understanding of the influence of environmental variation on the molecular systems of most ecologically relevant species as the pathways underlying fitness-affecting plastic responses have primarily been studied in model organisms under controlled laboratory conditions. In this study, we establish relationships between protein abundance patterns and the abiotic environment by profiling the proteomes of 24 natural populations of the caddisfly Crunoecia irrorata. We subsequently relate these profiles to natural variations in the abiotic characteristics of their freshwater spring habitats which shows that protein abundances and networks respond to abiotic variation according to the functional roles these proteins have. We provide evidence that geographic and past and present environmental differences between sites affect protein abundances and identifications, and that baseline reaction norms are ubiquitous and can be used as information rather than noise in comparative field studies. Taking this natural variation into account is a prerequisite if we are to identify the effects environmental change has on natural populations.

ecology

Diet-induced loss of adipose Hexokinase 2 triggers hyperglycemia

Chronically high blood glucose (hyperglycemia) leads to diabetes, fatty liver disease, and cardiovascular disease. Obesity is a major risk factor for hyperglycemia, but the underlying mechanism is unknown. Here we show that a high fat diet (HFD) in mice causes early loss of expression of the glycolytic enzyme Hexokinase 2 (HK2) specifically in adipose tissue. Adipose-specific knockout of Hk2 caused enhanced gluconeogenesis and lipogenesis in liver, a condition known as selective insulin resistance, leading to glucose intolerance. Furthermore, we observed reduced hexokinase activity in adipose tissue of obese and diabetic patients, and identified a loss-of-function mutation in the hk2 gene of naturally hyperglycemic Mexican cavefish. Mechanistically, HFD in mice led to loss of HK2 by inhibiting translation of Hk2 mRNA. Our findings identify adipose HK2 as a critical mediator of systemic glucose homeostasis, and suggest that obesity-induced loss of adipose HK2 is an evolutionarily conserved, non-cell-autonomous mechanism for the development of hyperglycemia. One Sentence SummaryLoss of the glycolytic enzyme Hexokinase 2 in adipose tissue is a mechanism underlying high blood glucose levels.

physiology