It is known that for
the preservation of muscle and an adequate level of physical performance during a restricted diet a minimum of 135 g of protein per day is necessary Transmembrane Transporters inhibitor for a subject of 80 kg. Eaton suggests that in ancestral humans, protein provided about 30% of daily energy intake (which corresponds to an intake of approximately 3 g/kg per day for a 70 kg individual consuming 12 500 kJ (3000 kcal)/d . In our study, it can be observed that despite a significant decrease of fat percentage and fat absolute amount, the strength performances remained stable after 30 days of VLCKD. Recently we have summarized the factors involved in the fat loss effect of VLCKD diets : 1. Satiety effect of proteins leading to appetite reduction in which also ketone bodies AZD8931 research buy may have a role, although the mechanism is not clear; 2. >Reduction in lipid synthesis and increased lipolysis mechanisms; 3. Reduction in at rest respiratory quotient and therefore an increase in fat metabolism for energy use; 4. Increased metabolic expenditure caused by gluconeogenesis and the thermic effect of proteins. The maintenance (or strictly speaking
the visible increase, albeit not significant) of the amount of lean body mass, muscle and percentage of muscle during the period of VLCKD needs to be underlined and this muscle sparing effect can be explained through the mechanism of ketosis. As stated before, fatty acids which are normally used as a major PTK6 fuel for some tissues such as muscle, cannot be used by the CNS because they cannot cross the blood–brain barrier. During starvation (fasting) this becomes a problem, particularly for organisms such as humans in which CNS metabolism constitutes a major portion of the resting basal metabolic rate (~20%). During the initial fasting period our body provides glucose for the metabolic needs of the CNS via break down of muscle tissue to provide the amino acid precursors
for gluconeogenesis. Obviously the organism could not survive long under such wasting conditions and ketone bodies (KB) therefore represent an alternate fat-based fuel source that spares muscle protein . It is noteworthy that the mechanism underlying the increase of body fat Cell Cycle inhibitor utilization has some pathways in common with mechanisms contributing to the lack of muscle mass increase. The use of FFA and ketones for muscle fuel spares muscle protein and is thus anti-catabolic. During the ketogenic period, whilst blood glucose decreases by a small amount, remaining at around 80–90 mg/dl, insulin remains at very low levels (7 mU/L) [58, 64, 65]. Insulin is involved in increased liposynthesis and decreased lipolysis so a reduction in insulin levels facilitates mobilization from fat stores; on the other hand insulin is fundamental for the muscle growth pathway (via IGF-1, mTOR, AKT etc.).