polyamine/obesity

To further evaluate the role of polyamines in insulin production and cell replication in diabetic pancreatic islets, we have studied hyperplastic islets of obese-hyperglycemic mice of different ages and normal islets of the same strain. The aims of the study were to investigate the impact of the

Blood polyamines (spermidine and spermine) and LH levels have been studied after acute GnRH injection both in obese and normal weight children. In both groups LH values significantly increased after stimulation but reached higher peaks in normal children than in obese ones (P less than 0.05). On the

BACKGROUND Obesity is associated with risks for mother and infant, and the mothers' dietary habits influence breast milk composition. Polyamines are secreted in breast milk and are essential for the regulation of intestinal and immune function in newborns and infants. The present study aimed to

BACKGROUND Polyamines (putrescine, spermidine, and spermine) are polycationic amines derived from arginine, which is the precursor of nitric oxide (NO). Due to the close relationship between the metabolism of polyamines and NO metabolism, the alteration in polyamine homeostasis can affect the NO

Previous studies from our laboratory demonstrate that polyamines, namely spermine and spermidine, stimulate adipose triacylglycerol formation from the sn-glycerol-3-phosphate pathway by activation of several enzymes from this pathway, including sn-glycerol-3-phosphate acyltransferase,

The polyamines putrescine, spermidine, and spermine are widely distributed polycationic compounds essential for cellular functions. Intracellular polyamine pools are tightly regulated by a complex regulatory mechanism involving de novo biosynthesis, catabolism, and transport across the plasma

Cellular metabolism is dynamically regulated in Natural Killer (NK) cells and strongly influences their responses. Metabolic dysfunction is linked to defective NK cell responses in diseases such as obesity and cancer. The transcription factors, sterol regulatory element binding protein (SREBP) and

The mitochondrial biogenesis and energy expenditure regulator, PGC-1α, has been previously reported to be induced in the white adipose tissue (WAT) and liver of mice overexpressing spermidine/spermine N (1)-acetyltransferase (SSAT). The activation of PGC-1α in these mouse lines leads to increased

Urinary polyamine excretion has been suggested to reflect hypermetabolism or catabolism in different illnesses. In the present study, the excretion of urinary polyamines was examined in 12 obese subjects (3 men, 9 women aged 32-55 y, body mass index 33.3-64.7 kg m-2) before and during a very low

BACKGROUND Chemoprevention with the polyamine-inhibitory regimen difluoromethylornithine (DFMO) + sulindac markedly reduces risk of recurrent adenoma in colorectal adenoma patients. Obesity is associated with risk of colorectal adenoma and colorectal cancer. This study investigates how obesity

Rapid synthesis of the polyamine catabolic enzyme spermidine/spermine-N(1)-acetyltransferase (SSAT) in response to increased polyamines is an important polyamine homeostatic mechanism. Indirect evidence has suggested that there is an important control mechanism involving the release of a

OBJECTIVE Cold and β3-adrenergic receptor (AR) agonists activate beige adipocyte biogenesis in white adipose tissue (WAT). The two stimuli also induce expression of inflammatory cytokines in WAT. The low-grade inflammation may further promote WAT browning. However, the mechanisms to reconcile these

Obesity is associated with lung function impairment and respiratory diseases; however, the underlying pathophysiological mechanisms are still elusive and therapeutic options are limited. This study examined the effects of prolonged excess fat intake on lung mechanics and microstructure and tested

BACKGROUND Lipocalin-2 is a proinflammatory adipokine upregulated in obese humans and animals. A pathogenic role of lipocalin-2 in hypertension has been suggested. Mice lacking lipocalin-2 are protected from dietary obesity-induced cardiovascular dysfunctions. Administration of lipocalin-2 causes