Objective: Hypertrophic obesity is associated with impaired insulin sensitivity and lipid-mobilizing activity of zinc-α2-glycoprotein. Adipose tissue (AT) of growth hormone (GH) -deficient patients is characterized by extreme adipocyte hypertrophy due to defects in AT lipid metabolism. It was hypothesized that zinc-α2-glycoprotein is regulated by GH and mediates some of its beneficial effects in AT.
Methods: AT from patients with GH deficiency and individuals with obesity-related GH deficit was obtained before and after 5-year and 24-month GH supplementation therapy. GH action was tested in primary human adipocytes. Relationships of GH and zinc-α2-glycoprotein with adipocyte size and insulin sensitivity were evaluated in nondiabetic patients with noncancerous cachexia and hypertrophic obesity.
Results: AT in GH-deficient adults displayed a substantial reduction of zinc-α2-glycoprotein. GH therapy normalized AT zinc-α2-glycoprotein. Obesity-related relative GH deficit was associated with almost 80% reduction of zinc-α2-glycoprotein mRNA in AT. GH increased zinc-α2-glycoprotein mRNA in both AT of obese men and primary human adipocytes. Interdependence of GH and zinc-α2-glycoprotein in regulating AT morphology and metabolic phenotype was evident from their relationship with adipocyte size and AT-specific and whole-body insulin sensitivity.
Conclusions: The results demonstrate that GH is involved in regulation of AT zinc-α2-glycoprotein; however, the molecular mechanism linking GH and zinc-α2-glycoprotein in AT is yet unknown.
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http://dx.doi.org/10.1002/oby.20856 | DOI Listing |
Biomark Med
January 2025
Neurology Department, University Hospital Fattouma Bourguiba, Monastir, Tunisia.
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View Article and Find Full Text PDFJ Clin Transl Endocrinol
December 2024
Division of Endocrinology Diabetes and Metabolism, Department of Medicine, University of Minnesota, Minneapolis, MN, USA.
Cystic fibrosis-related diabetes (CFRD) is the most common non-pulmonary comorbidity in people with cystic fibrosis (CF). Current guidelines recommend insulin therapy as the treatment of choice for people with CFRD. In the past, obesity and overweight were uncommon in individuals with CF.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
January 2025
National Metabolic Management Center, Longyan First Affiliated Hospital of Fujian Medical University, Longyan, Fujian, China.
Background: The triglycerides to Apolipoprotein A1 ratio (TG/APOA1) holds promise to be a more valuable index of insulin resistance for the diagnosis of metabolic dysfunction-associated fatty liver disease (MAFLD) in type 2 diabetes mellitus (T2DM). This study aims to evaluate the correlation between TG/APOA1 and MAFLD, as well as compare the efficacy of TG/APOA1 with triglycerides to high-density lipoprotein cholesterol ratio (TG/HDL-c) and triglyceride-glucose (TyG) index in identifying MAFLD among individuals with T2DM.
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Front Endocrinol (Lausanne)
January 2025
Department of Experimental Research, Guangxi Medical University Cancer Hospital, Nanning, China.
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View Article and Find Full Text PDFFront Endocrinol (Lausanne)
January 2025
Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, United States.
Diabetic cardiomyopathy (DMCM), defined as left ventricular dysfunction in the setting of diabetes mellitus without hypertension, coronary artery disease or valvular heart disease, is a well-recognized entity whose prevalence is certainly predicted to increase alongside the rising incidence and prevalence of diabetes mellitus. The pathophysiology of DMCM stems from hyperglycemia and insulin resistance, resulting in oxidative stress, inflammation, cardiomyocyte death, and fibrosis. These perturbations lead to left ventricular hypertrophy with associated impaired relaxation early in the course of the disease, and eventually culminating in combined systolic and diastolic heart failure.
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