Lecture 11

Everything that was covered in this lecture is in the PowerPoint file for the same lecture last year.

The only difference is that I managed to squeeze in the information on the different types of starches and on glycemic index (which, last year, were covered at the end of Lecture 7 and the beginning of Lecture8).

All the board shots are a little unnecessary – as the PowerPoint slides have the stuff much neater…. But here they are for good measure…

In the shot below, the only reason why the disaccharides are mentioned is that we discussed how the glycemic index can be a bit misinterpreted when the tested food contains carbohydrates other than starch/glucose. This is because sucrose is half fructose, lactose is half galactose and fructose is, well, fructose. Neither fructose nor galactose produce a big glycemic response (indeed, fructose can even be hypoglycemic).

In answer to several questions after the lecture, the reason why the addition of sucrose to a food LOWERS the GI is that GI testing is performed by measuring the post-meal glucose response to a PORTION OF THE FOOD THAT CONTAINS 50g OF CARBOHYDRATE - not a 50 g portion of the food. So to measure the GI of a food that contains 20% carbohydrate, one would eat 250 g of the food and the glucose area under the curve would then be compared to that elicited b a 50 g portion of glucose.

So, let’s suppose that the food mentioned above was starchy and had a GI of 80 – it might, for example, be a rice or potato product. If we now added sugar at, say, 10 g per 100 g, we now have a food that contains about 30% carbohydrate. So to eat a 50 g portion of carbs, we only need to eat 160 g…. and a much lower glycemic response will ensue.

OK, so now on to LIPOGENESIS. Generally covered in Chapter 19-4 of V&V – but in much more detail than our discussions.

We started with an overview….

Then talked about the first main step… activation of PDH

And seeing that PDH is a favourite enzyme of mine, I wanted to make sure everyone knew how important it was… hence lots of time spent on it’s irreversibility and control.

Page 517 in V&V (Section 16-2) provides all the detail on PDH… however, the structure reactions and involvement of ‘swinging arm’ transfers is all the stuff of Advanced lectures! It’s not until page 532 that we get the regulation of PDH – although this section does contain the extra useful information that acetyl CoA and NADH are important inhibitors of PDH and are activators of PDH kinase. This will become more important when we talk about starvation and exercise.

Then the fate of the acetyl CoA… condensation to citrate before either going into the Krebs Cycle or being exported out into the cytoplasm. The textbook is not really very informative when it comes to how acetyl CoA knows which pathway to go down… it’s basically determined by the relative activities of isocitrate dehydrogenase (which is the first rate limiting step of the Krebs Cycle) and ATP-citrate lyase (see next section).

And we discussed how the export was basically as citrate which was then cleaved in the cytoplasm to generate the acetyl CoA. This is discussed on p651 but, as with most textbooks, it is disappointing that they focus on how the oxaloacetate gets back into the mitochondria, rather than talking about the regulatory potential of this step.

We briefly discussed my disastrous TV appearance with reference to the supposed weight loss agent “hydroxy-citrate”.

And then on to the activation of acetyl CoA in readiness for the rounds of fatty acid synthesis.

The activation of the enzyme ACC by citrate and it’s inhibition by long chain fatty acids (or at least their CoA derivatives) is covered on p652. The assertion on p653 that “insulin activates ACC by dephosphorylating the enzyme” is at variance with my understanding [from Brownsey et al (2006) Biochem Soc Trans. 34:223-7] that insulin changes the pattern of phosphorylation. So, for exam purposes, we will just agree that insulin stimulates ACC by affecting the phosphorylation status of the enzyme.