EBR - Review Lesson

 

Review

The important thing to remember about the reading section of the SAT is that the answers are in the passage.  It's up to you to find the answers to the questions being asked. If the answers aren't explicitly stated, then there will be enough context clues available to answer the inference-based questions. One thing that will help you to focus more closely on the passage and to read more critically is to annotate the passage. The SAT will also focus on evidence based reading while utilizing the following question types: vocabulary words in context, command of evidence, informational graphics, and text complexity questions.

Use the following passage to help you prepare for the reading section of the SAT. Answer the questions following the passage. This passage is an example of how the reading section will focus on science based passages as well as utilize graphs and charts.

Scientists have known for more than 70 years that the one

surefire way to extend the lives of animals was to cut calories

by an average of 30 to 40 percent. The question was: Why?

Now a new study begins to unravel the mystery and the

Line 5    mechanism by which reducing food intake protects cells against

aging and age-related diseases.

Researchers report in the journal Cell  that the

phenomenon is likely linked to two enzymes—SIRT3 and

SIRT4—in mitochondria (the cell's powerhouse that, among

10         other tasks, converts nutrients to energy). They found that a

cascade of reactions triggered by lower caloric intake raises

the levels of these enzymes, leading to an increase in the

strength and efficiency of the cellular batteries. By

invigorating the mitochondria, SIRT3 and SIRT4 extend the

15         life of cells, by preventing flagging mitochondria from

developing tiny holes (or pores) in their membranes that

allow proteins that trigger apoptosis, or cell death, to seep out

into the rest of the cell.

"We didn't expect that the most important part of this

20         pathway was in the mitochondria," says David Sinclair, an

assistant professor of pathology at Harvard Medical School

and a study co-author. "We think that we've possibly found

regulators of aging."

In 2003 Sinclair's lab published a paper in Nature  that

25        described the discovery of a gene that switched on in the

yeast cell in response to calorie restriction, which Sinclair

calls a "master regulator in aging." Since then, his team has

been searching for an analogous gene that plays a similar role

in the mammalian cell.

30         The researchers determined from cultures of human

embryonic kidney cells that lower caloric intake sends a

signal that activates a gene inside cells that codes for the

enzyme NAMPT (nicotinamide phosphoribosyltransferase).

The two- to four-fold surge in NAMPT in turn triggers the

35         production of a molecule called NAD (nicotinamide adenine

dinucleotide), which plays a key role in cellular metabolism and signaling.

The uptick in NAD levels activates the SIRT3 and SIRT4

genes, increasing levels of their corresponding SIRT3 and

SIRT4 enzymes, which then flood the interior of the

40         mitochondria. Sinclair says he's not sure exactly how SIRT3

and SIRT4 beef up the mitochondria's energy output, but that

events leading to cell death are at the very least delayed when

there are vast quantities of the enzymes.

45                  SIRT3 and SIRT4 are part of a family called sirtuins

(SIRT1, which helps extend cell life by modulating the

number of repair proteins fixing DNA damage both inside

and outside the cell's nucleus, is also a member). SIRT is

short for sir-2 homologue—a well-studied protein that is

50         known to extend yeast cell longevity. According to Sinclair,

all of the mammalian SIRT genes (and their proteins) are

possible drug targets for therapies aimed at extending life, as

well as staving off age-related illnesses, such as Alzheimer's

disease, cancers and metabolic disorders, like diabetes.

55                  "I think SIRT3 is the next most interesting sirtuin from a

drug development standpoint," Sinclair says. "It does protect

cells, but there's growing evidence that it may mediate the

benefits of exercise as well."

Sinclair's lab is now working on developing what he calls

60         a possible "supermouse" with elevated levels of NAMPT to

see if it lives longer and is more disease-resistant than normal

mice.

Matt Kaeberlein, a pathologist at the University of

Washington in Seattle, says that Sinclair's team has an

interesting hypothesis connecting the mitochondria to

longevity, but that it needs to be more directly tested in the

context of dietary restriction. "If the NAMPT-overexpressing

mice are long-lived and disease resistant, that will provide

more support for this idea."

 

Lifespan of Groups of Mice With Different Levels of Caloric Reduction

 

 

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