Charles A Harris's research while affiliated with Washington University in St. Louis and other places

... The role of leptin in muscle mass has been recently confirmed in a study conducted in fat-free lipodystrophic mice with decreased muscle mass and strength, in which a full rescue of muscle mass, in term of quantity and function, was observed after replacement of just ∼10% of normal WAT, and in which this effect was shown to be independently due to leptin and separable from the reversal of systemic metabolic derangement [151]. ...

... Moreover, transplants of subcutaneous AT prevent ectopic BMAd expansion in fat-free mice. Although previously underestimated, this study indicates the important role of BMAT in lipid storage [9]. Importantly, reduced lipolysis and a cholesterolbased metabolism has been reported in human BMAds when compared to subcutaneous adipocytes [10]. ...

... In a 2021 study, Collins et al. evaluated the relationship between the gut microbiota and knee cartilage damage using lipodystrophic (LD) mice, which are protected from obesityassociated OA associated with HFD [60]. Interestingly, in these mice, the OA trait can be "rescued" by implantation of a small amount of wild-type fat tissue subcutaneously into LD mice [61]. ...

... After this, Leilei Zhong presented new data that defines a stromal/ perivascular, adiponectin-expressing bone marrow adipocyte progenitor, termed the marrow adipogenic lineage precursor (MALP) and its role in the maintenance of the bone marrow vasculature (34,35). Last, Xiao Zhang showed that a unique population of maladapted bone marrow adipocytes was retained in an otherwise 'fat free' lipodystrophic mouse, revealing the existence of a bone-specific, compensatory adipogenesis pathway that is activated in states of metabolic stress (36). Overall, this session contributed to our understanding of the unique cellular origins of bone marrow adipocytes during development and metabolic disease, in addition to providing new information about the molecular signals regulating the maturation of committed pre-adipocytes within the bone marrow. ...

... Adipocytes also produce adipokines, a type of cytokine known to promote synovial inflammation, attract cartilage-degrading enzymes, and enhance bone matrix remodeling. Adipokines have been shown to accumulate in joints such as the knee, hip, elbow, and ankle with aging and obesity [97,98]. Adipokines such as leptin, adiponectin, and resistin are known to be associated with joint degradation and are thought to drive chronic inflammatory processes [99,100]. ...

... Carbohydrates and lipids are the main sources of energy required by organisms to maintain life activities. The homeostasis imbalance of the regulatory network is also an important inducing factor for the occurrence and development of a variety of metabolic diseases [1][2][3]. Glucose and lipid metabolism disorder is the main clinical phenotype of obesity, type 2 diabetes and nonalcoholic fatty liver disease, and can also induce cardiovascular and cerebrovascular diseases [4]. Under the influence of genetic and/or environmental factors, the decrease of insulin secretion or the disturbance of signal transduction (insulin resistance) will lead to the decrease of energy supply from glucose sources and the enhancement of lipid decomposition and release, and can stimulate liver gluconeogenesis, promote liver glucose release, and participate in the occurrence and development of diabetes and its complications [5,6]. ...

... Notably, myosteatosis indicates pathological fat infiltration in muscles and is considered to be a distinct entity from loss of muscle quantity [36]. It has been suggested that myosteatosis is in close relation to muscle fiber disarrangement, thus disrupting muscle contractility and weakening mechanical action [37,38]. Accordingly, Sugiyama et al. showed that patients with cirrhosis and dynapenia present with high BMI and myosteatosis [39]. ...

... BAT is a thermogenic adipose tissue that metabolizes fatty acids and glucose and dissipates the stored chemical energy in the form of heat (Basse et al., 2015). Thermogenesis depends on a high mitochondrial density and expression of Uncoupling protein 1 (Ucp1), and serves as protection from hypothermia and, potentially, obesity (Basse et al., 2015;Craft et al., 2019). In addition to UCP1 protein expression, BAT is also characterized by expression of marker genes such as Pparg, PR domain containing 16 (Prdm16) and Peroxisome proliferator-activated receptor γcoactivator 1α (Ppargc1a, sometimes referred to as Pgc1a) (Bukowska et al., 2018). ...

... However, the exact role of white adipocyte MR in obesity and its associated metabolic disorders remains uncertain. Several studies using genetic adipocyte-specific MR overexpression or knockout mice have revealed a deteriorative effect of adipocyte MR on the regulation of obesity-related metabolic disorders [112,119,120] . However, two other studies have shown that the depletion of MR in mature adipocytes exerts minor to modest improvements on obesity-associated glucose intolerance, insulin resistance, and hepatic steatosis [121,122] . ...

... On the one hand, adipocytes produce adipokines, such as leptin and adiponectin, that suppress osteoblast function and lead to bone loss (40)(41)(42). This interaction may partially explain the robust bone formation that occurs in "fat-free" mice (43). On the other hand, the storage of triglycerides in mature adipocytes represents a potential energy supply for bone formation. ...