Ketogenesis supports hepatic polyunsaturated fatty acid homeostasis via fatty acid elongation.

Ketogenesis is a dynamic metabolic conduit supporting hepatic fat oxidation particularly when carbohydrates are in short supply. Ketone bodies may be recycled into anabolic substrates, but a physiological role for this process has not been identified. Here, we use mass spectrometry-based C-isotope tracing and shotgun lipidomics to establish a link between hepatic ketogenesis and lipid anabolism.

Cognitive impairment caused by compromised hepatic ketogenesis is prevented by endurance exercise.

Extensive research has demonstrated endurance exercise to be neuroprotective. Whether these neuroprotective benefits are mediated, in part, by hepatic ketone production remains unclear. To investigate the role of hepatic ketone production on brain health during exercise, healthy 6-month-old female rats underwent viral knockdown of the rate-limiting enzyme in the liver that catalyses the first reaction in ketogenesis: 3-hydroxymethylglutaryl-CoA synthase 2 (HMGCS2).

A study of sheep scab in Northern Ireland including detection and identifying barriers to control.

Background: Sheep scab, caused by the highly infectious mite, is considered to be endemic in Northern Ireland, although little investigation has been reported. A pilot project was undertaken to engage farmers, confirm cases with diagnostic methods and identify specific barriers to control, with the aim of informing future control programmes.

Methods: Through farmers self-reporting suspected outbreaks, on-farm risk assessments and clinical investigations were carried out by the farm's veterinary surgeon, who utilised light microscopy and serological testing to diagnose scab.

Deciphering Colorectal Cancer-Hepatocyte Interactions: A Multiomic Platform for Interrogation of Metabolic Crosstalk in the Liver-Tumor Microenvironment.

Metabolic reprogramming is a hallmark of cancer, enabling tumor cells to adapt to and exploit their microenvironment for sustained growth. The liver is a common site of metastasis, but the interactions between tumor cells and hepatocytes remain poorly understood. In the context of liver metastasis, these interactions play a crucial role in promoting tumor survival and progression.

Dietary Restriction Enhances CD8 T Cell Ketolysis to Limit Exhaustion and Boost Anti-Tumor Immunity.

Reducing calorie intake without malnutrition limits tumor progression but the underlying mechanisms are poorly understood. Here we show that dietary restriction (DR) suppresses tumor growth by enhancing CD8 T cell-mediated anti-tumor immunity. DR reshapes CD8 T cell differentiation within the tumor microenvironment (TME), promoting the development of effector T cell subsets while limiting the accumulation of exhausted T (Tex) cells, and synergizes with anti-PD1 immunotherapy to restrict tumor growth.