Gizmag: Injectable nanoparticles maintain normal blood-sugar levels for up to 10 days.

Fascinating technology featured in Gizmag & posted by someone HERE.

The nano-network that releases insulin in response to changes in blood sugar

"The injectable nano-network is made up of a mixture that contains nanoparticles with a solid core or insulin, modified dextran (which is commonly used to reduce blood viscosity), and glucose oxidase enzymes. When exposed to high levels of glucose, the enzymes convert glucose into gluconic acid, which breaks down the modified dextran to release the insulin. The gluconic acid and dextran, which are biocompatible, dissolve in the body, while the insulin brings the glucose levels under control.

The nanoparticles are given a positively or negatively charged biocompatible coating so that when they are mixed together, they are attracted to each other to form a “nano-network.” The positively charged coatings are made of chitosan, a material found in shrimp shells that has also found applications in self-healing car paint, while the negatively charged coatings are made of alginate, a material normally found in seaweed."

Wow! Cool bananas!

Metabolic Inflexibility: What it really means.

Here's a picture from Metabolic Flexibility and Insulin Resistance.

The Metabolically-Inflexible (MI) & Insulin Resistance

Here's another picture.

Fig 2. ● = Metabolically-Flexible (MF). ○ = Metabolically-Inflexible (MI).

Salient points:
1) Excess serum FFA a.k.a. NEFA is bad.
2) Respiratory Quotient (RQ) a.k.a. Respiratory Exchange Ratio (RER) changes due to dietary changes are more sluggish in the MI than in the MF.
3) Under Insulin Clamp conditions, RQ/RER is lower in the MI than in the MF, due to impairment of glucose oxidation and non-oxidative glucose disposal.

I have posted this because of Danny Roddy's post Is Supplemental Magnesium A Surrogate For Thyroid Hormone? , which leads onto A Bioenergetic View of High-Fat Diets.

In the first article, Danny Roddy writes:-
"Additionally, taking magnesium while actively engaging in a diet or lifestyle that reduces the respiratory quotient (e.g., high-fat diet, light deficiency, excessive exercise) seems pretty silly. For example, as a rule, diabetics have a reduced respiratory quotient (Simonson DC, et al. 1988), tend to have higher levels of free fatty acids or NEFA (Kahn SE, 2006), and are often deficient in magnesium (De Valk HW, 1999)."

The second sentence (diabetics have a reduced respiratory quotient...and are often deficient in magnesium) seems to contradict the first sentence (...taking magnesium while actively engaging in a diet or lifestyle that reduces the respiratory quotient seems pretty silly).

Simonson DC, et al. 1988 is Oxidative and non-oxidative glucose metabolism in non-obese type 2 (non-insulin-dependent) diabetic patients.
"In conclusion, during the postabsorptive state and under conditions of euglycaemic hyperinsulinaemia, impairment of glucose oxidation and non-oxidative glucose disposal both contribute to the insulin resistance observed in normal weight Type 2 diabetic patients. Since lipid oxidation was normal in this group of diabetic patients, excessive non-esterified fatty acid oxidation cannot explain the defects in glucose disposal."

Impaired glucose oxidation with normal lipid oxidation lowers RQ/RER. Therefore, lower RQ/RER must be bad, right? Wrong. From the above study:-
"...euglycaemic insulin clamp studies were performed..."
Remember Salient point 3)? Simonson DC, et al. 1988 is an insulin clamp study, the results of which don't apply to free-living people (who aren't insulin clamped).

See also Determinants of the variability in respiratory exchange ratio at rest and during exercise in trained athletes. RER/RQ increases & decreases with increases & decreases in exercise intensity. This is Metabolic Flexibility (MF). Sorry, Danny.

Uh-oh! There may be trouble ahead...

I won't deny that I'm not very active. On days that I don't visit my mum, I spend many hours reclining on a sofa with a lap-top on a small table, surfing the internet. I make sloths look hyperactive!

I thought that this wasn't a problem as I also don't eat very much (as I'm so engrossed rummaging through the vast amount of information out there) and I'm maintaining a relatively stable weight.

Then I read Sedentary Physiology at Obesity Panacea which lead me to Sedentary Physiology Part 1 – Not Just The Lack of Physical Activity , full study HERE.

"Hamburg et al. (2007) examined the effect of 5 days of complete bed rest on metabolic health in 22 adult volunteers. Study participants remained in bed for over 23.5 h per day, rising only for matters of personal hygiene. At the completion of the study, despite no changes in body weight, they experienced significant increases in total cholesterol, plasma triglycerides, glucose, and insulin resistance. The changes in carbohydrate metabolism were particularly pronounced, with participants experiencing a 67% greater insulin response to a glucose load following the 5-day intervention."

The thing is, I've never liked sports & formal exercise. In infant school, exercise involved running around in the playground. That, I could do. In primary school, exercise involved running around in the playground, some PE and some outdoor sports (rounders & cricket, using a tennis ball). That, I could also do, although my short legs made me rubbish at running. In secondary school, in addition to PE, there were sports such as football, rugby, cricket, hockey, tennis, swimming & cross-country running. That, I utterly hated (tennis was just about bearable) and so to avoid doing them, I developed an art for forging sick notes in my mum's handwriting. This improved my normal handwriting, so some good came of it. So, what to do?

As toilet breaks force me off the sofa, I shall drink more to make me wee more often. I shall also use the upstairs toilet during the day and the downstairs toilet during the night. See also Eat Less, Move More: Solutions to problems.

Natural & synthetic disaccharides.

As mentioned in Carbohydrates: Dogs' Doodads or Spawn of Satan?, there are three common disaccharides, sucrose (table sugar), lactose (milk sugar) and maltose (beer sugar). These all contain a molecule of glucose linked by a glycosidic bond to molecules of fructose, galactose and glucose respectively. In our bodies, our guts contain the enzymes sucrase, lactase & maltase which hydrolyse the glycosidic bond breaking the disaccharides into their constituent monosaccharides. People who lack any of these enzymes are unable to break the disaccharide into monosaccharides. As disaccharides are not absorbed, they pass along the gut until they reach the colon, where colonic bacteria ferment the disaccharides into short-chain fatty acids and gas. This increases ammonia levels in the colon which attracts water. End result: Lots of gas, soft poo and the excretion of ammonia (nitrogenous waste).

There's a synthetic disaccharide called lactulose, which is a disaccharide of fructose and galactose. As our bodies don't contain the enzyme lactulase, lactulose is fermented, producing lots of gas & soft poo. I thought I'd post about this as I'm taking lactulose to prevent the constipation caused by high dose Co-Codamol, the pain-killer I'm on while my 4-inch scar heals. It works!

An interesting but otherwise useless fact: The artificial sweetener sucralose that's made from & is about 600 times sweeter than sugar has the chemical name 1,6-Dichloro-1,6-dideoxy-β-D-fructofuranosyl-4-chloro-4-deoxy-α-D-galactopyranoside (I'm nerdy enough to know that by heart!). Sucralose has a structure like lactulose rather than sucrose, which has the chemical name β-D-fructofuranosyl-(2→1)-α-D-glucopyranoside. As the amount of sucralose used is about one 600th that of sucrose, it doesn't cause the above effects.