Publications by authors named "I D Goldfine"

Diabetes mellitus is a complex disease. We are increasingly gaining a better understanding of its mechanisms at the molecular level. From these new insights, better therapeutic approaches should emerge.

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Background: Insulin resistance in visceral adipose tissue (VAT), skeletal muscle and liver is a prominent feature of most patients with obesity. How this association arises remains poorly understood. The objective of this study was to demonstrate that the decrease in insulin receptor (INSR) expression and insulin signaling in VAT from obese individuals is an early molecular manifestation that might play a crucial role in the cascade of events leading to systemic insulin resistance.

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Loss-of-function mutations of the ß-cell ATP-sensitive potassium channels (K) cause the most common and severe form of congenital hyperinsulinism (KHI), a disorder of ß-cell function characterized by severe hypoglycemia. Children with KHI are typically unresponsive to medical therapy and require pancreatectomy for intractable hypoglycemia. We tested the hypothesis that inhibition of insulin receptor signaling may prevent hypoglycemia in KHI.

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Article Synopsis
  • * Liver biopsy is the best method for diagnosing NAFLD and differentiating between simple steatosis and the more severe non-alcoholic steatohepatitis (NASH), although the exact causes of NASH are still not fully understood.
  • * New treatments are being explored, including vitamin E and the synthetic recombinant protein rMnSOD, which shows promise as a powerful antioxidant that can help reduce liver-related complications by addressing oxidative stress and fibrosis.
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Background: Cerebral salt-wasting syndrome (CSWS) was initially described over 60 years ago in hyponatremic patients with a cerebral lesion. However, the diagnostic criteria for CSWS have not been fully established. Thus, when hyponatremia is observed in patients with CSWS, they may be misdiagnosed as having the syndrome of inappropriate secretion of antidiuretic hormone (SIADH).

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