05 | October | 2019 | Boomers Daily

From a Cell Metabolism online release:

In summary, dietary fructose, but not glucose, supplementation of HFD impairs mitochondrial size, function, and protein acetylation, resulting in decreased fatty acid oxidation and development of metabolic dysregulation.

Dietary sugars, fructose and glucose, promote hepatic de novo lipogenesis and modify the effects of a high-fat diet (HFD) on the development of insulin resistance. Here, we show that fructose and glucose supplementation of an HFD exert divergent effects on hepatic mitochondrial function and fatty acid oxidation. This is mediated via three different nodes of regulation, including differential effects on malonyl-CoA levels, effects on mitochondrial size/protein abundance, and acetylation of mitochondrial proteins. HFD- and HFD plus fructose-fed mice have decreased CTP1a activity, the rate-limiting enzyme of fatty acid oxidation, whereas knockdown of fructose metabolism increases CPT1a and its acylcarnitine products. Furthermore, fructose-supplemented HFD leads to increased acetylation of ACADL and CPT1a, which is associated with decreased fat metabolism.

From a San Francisco Chronicle online article:

As trivia game experts know, San Francisco has had three U.S. mints. The first mint, on Commercial Street, was replaced in 1874 by a grand structure at Fifth and Mission streets. That building, now called the Old Mint, was itself replaced in 1937 by a new mint on Duboce Avenue, which is still coining money,

The newest museum in San Francisco will open in the city’s oldest mint this week.

The Commercial Street building is built on the site of the first U.S. mint in the West, which opened in 1854 during the California Gold Rush to turn nuggets and gold dust into coins and bullion. Later it was used as a subtreasury, where the government stored millions of dollars in gold and silver bars.