The invention relates to the field of obesity and related metabolic diseases. More specifically, the invention relates to methods of reducing aggrecanase activity or antigen in mammals in order to enhance brown adipose tissue (BAT) development, to promote conversion of white adipose tissue (WAT) into BAT in vivo, and to limit triglyceride accumulation and steatosis in the liver. The invention also relates to a strategy of neutralization or depletion of ADAMTS5 as a strategy to inhibit adipogenesis and more specifically, the invention relates to a method of reducing aggracanase-2 (ADAMTS5, A Disintegrin and Metalloproteinase with Thrombospondin motif 1; member 5) antigen and/or activity in mammals in order to impair differentiation of precursor cells into mature adipocytes (i.e., adipogenesis).

The present invention relates to a method of providing a FAS finding (30) for the functionality of an anorexigenic signal path for a patient, comprising the steps: providing a sample matrix (10) of a body substance of the patient, determining at least one first FAS indicator (11) from the sample matrix (10), determining at least one second FAS indicator (12) from the sample matrix (10), wherein the at least one second FAS indicator (12) is different from the at least one first FAS indicator (11), and generating the FAS finding (30) using an indicator spectrum (20) comprising the at least one first FAS indicator (11) and the at least one second FAS indicator (12). The invention also relates to an analysis device (100) for providing a FAS finding (30) with a computer program product according to the invention (90) and a storage means (80) with a computer program product (90) according to the invention stored thereon.

Disclosed herein are insulin resistance reporters for use in quantifying insulin response in biological cells. These biological cells may be stem cell compositions or derivatives thereof comprising the insulin resistance reporter. The stem cell derivatives include but are not limited to insulin responsive cells, tissues, or organoids, such as pancreatic, brain, adipose, muscle, or liver cells, or tissues or organoids thereof. Also disclosed herein are methods of using said insulin resistance reporters and cells with these insulin resistance reporters as models to examine insulin resistance and screening for compounds that are potentially useful for the treatment of diseases or disorders associated with insulin resistance. The cells comprising an insulin resistance reporter may be hepatic cells or liver organoid compositions, which can be used in investigating hepatic insulin resistance, for example, as a result of non-alcoholic fatty liver disease or steatohepatitis.

The present invention relates to a method of providing an FAS finding (30) for the functionality of an anorexigenic signal path for a patient (1). Said method comprises the following steps: placing the patient (1) in a normalised preparation state in preparation for a normalised sample collection, providing a normalised sample matrix (10) collected from a patient (1) who was in the normalised preparation state, and determining at least one FAS indicator (11, 12, 13) from the normalised sample matrix (10), generating the FAS finding (30) based on the at least one determined FAS indicator (11, 12, 13).

The disclosure provides for methods, compositions and kits that utilize total Oxidized phospholipids to determine whether a subject has liver disease.

The present invention identifies AKR1C1 as the first lipedema-associated gene. The invention provides methods for diagnosing or assessing an individual's susceptibility to lipedema by the analysis of the AKR1C1 gene or the expression levels of its product and related metabolites. Also provided are therapeutic methods for treating a patient or methods for prophylactically treating an individual susceptible to lipedema.

Methods and compositions for treating Gaucher disease are described.

The present invention relates to a method for measuring the cholesterol uptake capacity of lipoproteins. The present invention also relates to a reagent kit for measuring the cholesterol uptake capacity of lipoproteins. The present invention further relates to a tagged cholesterol which can be used in the method and the reagent kit.

The invention provides methods of assessing unbound PCSK9 or effective PCSK9 activity in a subject based on the novel insights of the inventors that high levels of PCSK9 are bound to HDL in vivo and that this HDL can activate PCSK9 function. Specifically depleting HDL from a sample from a subject allows improved assessment of the level of unbound PCSK9. The invention provides such analytical methods, plus also associated methods of treatment and related kits.

This disclosure relates to uses of 5-aminovaleric acid betaine and compositions related thereto. In certain embodiments, this disclosure relates to diagnostic assays and methods of measuring and monitoring 5-aminovaleric acid betaine levels or the ratio 5-aminovaleric acid betaine to carnitine in a sample. In certain embodiments, this disclosure relates to methods of treating or preventing muscle wasting comprising administering to a subject in need thereof an effective amount of 5-aminovaleric acid betaine, prodrug, or salt thereof