Nutrition
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Case Reports
Acute thiamine deficiency and refeeding syndrome: Similar findings but different pathogenesis.
Refeeding syndrome can occur in several contexts of relative malnutrition in which an overaggressive nutritional support is started. The consequences are life threatening with multiorgan impairment, and severe electrolyte imbalances. During refeeding, glucose-involved insulin secretion causes abrupt reverse of lipolysis and a switch from catabolism to anabolism. This creates a sudden cellular demand for electrolytes (phosphate, potassium, and magnesium) necessary for synthesis of adenosine triphosphate, glucose transport, and other synthesis reactions, resulting in decreased serum levels. Laboratory findings and multiorgan impairment similar to refeeding syndrome also are observed in acute thiamine deficiency. The aim of this study was to determine whether thiamine deficiency was responsible for the electrolyte imbalance caused by tubular electrolyte losses. ⋯ Our study indicates that, despite sharing many laboratory similarities, refeeding syndrome and acute thiamine deficiency should be viewed as separate entities in which the electrolyte abnormalities reported in cases of refeeding syndrome with thiamine deficiency and refractory lactic acidosis may be due to renal tubular losses instead of a shifting from extracellular to intracellular compartments. In oncologic and malnourished patients, individuals at particular risk for developing refeeding syndrome, in the presence of these biochemical abnormalities, acute thiamine deficiency should be suspected and treated because it promptly responds to thiamine administration.
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St. John's Wort (SJW) extract, which is commonly used to treat depression, inhibits the reuptake of several neurotransmitters, including glutamate, serotonin, norepinephrine, and dopamine. Glutamatergic visceral vagal afferents synapse upon neurons of the solitary tract (NST); thus, the aim of this study was to evaluate whether SJW extract modulates glutamatergic neurotransmission within the NST. ⋯ These data suggest that SJW extract can significantly increase the probability of glutamate release from vagal afferents onto the NST by increasing presynaptic calcium. The in vitro vagal afferent synapse with NST neurons is an ideal model system to examine the mechanism of action of botanical agents on glutamatergic neurotransmission.
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The objective of this study was to compare the profiles of proinflammatory (interleukin [IL]-6 and tumor necrosis factor [TNF]) and anti-inflammatory (IL-10 and transforming growth factor [TGF]-β) adipokines in the blood, subcutaneous adipose tissue (SAT), and visceral adipose tissue (VAT) of metabolically healthy class III obese individuals and normal-weight controls. ⋯ Metabolically healthy, extremely obese individuals have effective immunoregulation to counter chronic obesity-related inflammation through the increased production of the anti-inflammatory cytokines IL-10 and TGF-β in adipose tissue, especially SAT; the increased presence of FOXP3-positive regulatory T cells; and increases in angiogenesis and adipogenesis induced by TGF-β and MMPs. These regulatory mechanisms could be important in the delayed onset of metabolic complications, even in extremely obese individuals.
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Plant-based therapies have been used in medicine throughout recorded history. Information about the therapeutic properties of plants often can be found in local cultures as folk medicine is communicated from one generation to the next. The aim of this study was to identify native Louisiana plants from Creole folk medicine as a potential source of therapeutic compounds for the treatment of insulin resistance, type 2 diabetes, and related disorders. ⋯ An interdisciplinary approach to screening botanical sources of therapeutic agents can be successfully applied to identify native plants used in folk medicine as potential sources of therapeutic agents in treating insulin resistance in skeletal muscle or inflammatory processes associated with obesity-related insulin resistance.
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The aim of this study was to evaluate the effects of resistance exercise on the mRNA expression of muscle mammalian target of rapamycin (mTOR), muscle-specific RING finger-1 (MuRF-1), and muscle atrophy F-box (MAFbx) in the presence or absence of whey protein ingestion. We hypothesized that resistance exercise in combination with whey protein ingestion alters the gene expression of proteins related to muscle protein synthesis (mTOR) and/or degradation (MuRF-1 and MAFbx), thus affecting muscle weight gain in rats. ⋯ A reduction in MAFbx gene transcription induced by whey protein and the interaction between exercise and whey protein ingestion on mTOR gene expression contributed significantly to differences in body and muscle weight gain.